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Foundations of Medicine > Immunology > Flashcards

Immunology Flashcards

1
Q

What is inflammation?

A

Tissue damage initiates a set of vascular and cellular events that are designed to be able to clean up cellular debris, and infectious organisms and initiate repair.

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2
Q

What causes inflammation?

A

Physical trauma, chemical trauma, infectious organisms, sunlight and burns, and allergies.

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3
Q

What are the 2 divisions of the Immune System?

A

Innate (Natural) Immunity and Acquired (Adaptive) Immunity

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4
Q

How can you manipulate the immune system to prevent or treat human diseases?

A
  1. Immunization
  2. Anti-inflammatory and Immunosuppressive drugs.
  3. Cancer immunotherapy
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5
Q

What does cancer immunotherapy enables?

A

Immunotherapy enables the immune system to recognize, target and eliminate cancer cells, making it a potential ‘universal answer’ to cancer.

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6
Q

What are soluble factors?

A

They are factors which sense, either directly or indirectly, the potential threats and produce inflammation and cellular death.

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7
Q

What are the soluble factors of Innate Immunity?

A
  1. Cytokines
  2. Acute Phase Proteins
  3. Inflammatory Mediators
  4. Complement Proteins
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8
Q

What are the immune cells involved in Innate Immunity?

A
  1. Mast cells
  2. Natural Killer Cells
  3. Macrophages
  4. Dendritic cells
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9
Q

What is Innate Immunity?

A

It is a defense mechanism that is present from birth and is generally non-specific

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10
Q

What is the Acquired Immunity?

A

It is a defense mechanism induced by the presence of foreign or non-self material (including infectious microorganisms).
The response is unique to the specific substance or pathogen that induced the response.

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11
Q

What are the soluble factors of Acquired Immunity?

A
  1. Cytokines
  2. Antibodies
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12
Q

What are the Immune Cells involved in Acquired Immunity?

A
  1. B cells
  2. T cells
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13
Q

What are the four pathogens’ routes of entry?

A
  1. Digestive System
  2. Respiratory System
  3. Urogenital System
  4. Skin damage
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14
Q

What are the two routes of attack?

A
  1. Circulatory System
  2. Lymphatic System
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15
Q

Tell me the 6 barriers to infection

A
  1. Physical Barrier
  2. Traps
  3. Unfavorable pH
  4. Elimination
  5. Lysozyme enzyme
  6. Commensal bacteria
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16
Q

What are the physical barriers?

A

Skin and mucosal membrane lining in DIGESTIVE, URINARY, RESPIRATORY

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17
Q

What traps are there?

A

Mucous, cilia (Nose & Trachea), hair (covering body & in nose and ears), earwax

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18
Q

What Elimination barriers are there?

A

Coughing, sneezing, urination, and diarrhea

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19
Q

Where is the unfavorable pH?

A

Stomach Acid, sweat, saliva, urine

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20
Q

What do lysozyme enzymes do, and where can you find them?

A

It acts as an antimicrobial agent by cleaving the peptidoglycan component of bacterial cell walls (Digests bacterial walls), leading to cell death; Tears, and sweat

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21
Q

What are the four fundamental properties of adaptive immunity?

A
  1. Specificity
  2. Adaptiveness
  3. Distinguishing between self and non-self
  4. Memory
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22
Q

How long does Innate and Acquired immunity take to respond?

A
  • Innate: Rapid response, mins-hrs
  • Acquired: Slow response, days
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23
Q

Which tissue-resident innate immune cells recognize pathogens as non-self?

A
  • Phagocytic cells (Macrophages and Dendritic cells)
  • Mast cells
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24
Q

How are pathogens identified?

A

Pathogens express unique structures that are not present on/in human cells (PAMPs, pathogen-associated molecular patterns)

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25
Q

What does PAMPS stand for?

A

Pathogen-Associated Molecular Patterns

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26
Q

How do Innate Immune cells pick pathogens up?

A

They express partner receptors, Pattern Recognition Receptors (PRRs)

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27
Q

What does PRRs stand for?

A

Pattern Recognition Receptors.

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28
Q

Do non-immune cells also express PRRs?

A

Yes, intracellularly. To recognize if they have been infected by intracellular pathogens such as viruses.

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29
Q

Tell me the 3 modes of ingestion

A
  1. Pinocytosis: Ingestion of extracellula fluid surrounding the cells.
  2. Receptor-mediated endocytosis: Molecules bound to membrane receptors are internalized
  3. Phagocytosis: Intact particles are internalized as a whole.
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30
Q

What is an important step in Acquired Immunity?

A

Receptor-mediated endocytosis

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31
Q

What is opsonization, and what happens without it?

A

Opsonization is an immune process that uses opsonins to tag foreign pathogens for elimination by phagocytes. Without an opsonin, such as an antibody, the negatively-charged cell walls of the pathogen and phagocyte repel each other.

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32
Q

Three examples of opsonins

A
  1. C3b
  2. C-reactive protein (CRP)
  3. IgG/IgM
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33
Q

Tell me the seven steps of PHAGOCYTOSIS

A
  1. Macrophages express PRRs
  2. Receptor binding to PAMPs signals the formation of a phagocytic cup.
  3. Cup extends around the target and pinches off, forming a PHAGOSOME.
  4. Fusion with lysosomes to form a PHAGOLYSOSOME- killing pathogens and degrading contents through acidification.
  5. Debris (Including antigens) is released into the extracellular fluid
  6. Pathogen-derived peptides are expressed on special cell surface receptors (MHC-II molecules)
  7. Pro-inflammatory mediators are released
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34
Q

What phagocytosis is a specific form of?

A

Endocytosis

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35
Q

Which are the professional phagocytes of the immune system?

A

Macrophages, neutrophils, and immature dendritic cells.

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36
Q

Do parasites undergo phagocytosis?

A

No, they are too large

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37
Q

What do mast cells do?

A
  1. Degranulation: Release of pre-formed pro-inflammatory substances (e.g, histamine)
  2. Gene expression: Production of new pro-inflammatory substances (e.g, leukotrienes, prostaglandins)
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38
Q

What are the four pro-inflammatory mediators?

A
  1. Nitric Oxide
  2. Prostaglandins/ leukotrienes
  3. Histamines
  4. Pro-inflammatory cytokines (TNFα)
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39
Q

What three things inflammation promote?

A
  1. Vascular changes.
  2. Recruitment and activation of neutrophils (transendothelial migration).
  3. Bacteria produce chemicals that attract neutrophils to the site of infection.
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40
Q

What four changes are promoted in normal vasculature?

A
  1. Vasodilation and increased blood flow (rubor)
  2. Increased vascular permeability (swelling/edema)
  3. Expression of specific adhesion molecules on the surface of the endothelial cells.
  4. Activation of adhesion molecule receptors on circulating neutrophils
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41
Q

What are the five steps of transendothelial migrations?

A
  1. Margination of neutrophils to the endothelium near sites of tissues damage/infection
  2. Binding of neutrophils to adhesion molecules (selectins, ICAM-1) on the endothelial cells.
  3. Migration of neutrophils across the endothelium via the process of diapedesis.
  4. Movement of neutrophils within the tissue via chemotaxis.
  5. Activation of neutrophils by PAMPs and TNFα
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42
Q

What do neutrophils do?

A
  1. Phagocytosis
  2. Degranulation
  3. NETs
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43
Q

Which two distinct mechanisms do neutrophils kill internalized pathogens?

A

Phagolysosomal killing and ROS-dependent killing

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44
Q

What are the four steps of Phagolysosomal killing?

A
  1. Bacterium is phagocytosed by neutrophil
  2. Phagosome fuses with azurophilic and specific granules.
  3. pH of the phagosome rises, the antimicrobial response is activated, and the bacterium is killed
  4. pH of phagosome decreases and fusion with lysosomes allows acid hydrolases to degrade the bacterium completely.
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45
Q

What are the three steps of ROS-dependent killing?

A
  1. Neutrophil activation (PAMPs, pro-inflammatory cytokines)
  2. Assembly of the NADPH oxidase complex
  3. Production and release of ROS into the phagolysosome
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46
Q

What does ROS stand for?

A

Reactive Oxygen Species

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47
Q

What do neutrophils do in degranulation?

A

Release of anti-bacterial proteins from neutrophil granules directly into the extracellular milieu.

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48
Q

What happens when neutrophils degranulate?

A
  1. There is a direct killing of extracellular pathogens, bacteria, and fungi.
  2. Tissue damage and (potentially) systemic inflammation.
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49
Q

What are NETs?

A

Neutrophil extracellular traps (NETs) are networks of extracellular fibers, primarily composed of DNA from neutrophils, which bind pathogens.

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50
Q

What is the Acute Phase Response?

A

The acute phase response is a group of physiological processes occurring soon after the onset of infection, trauma, and inflammatory processes. These include increased acute phase proteins in serum, fever, and vascular permeability. Metabolic and pathologic changes protect against tissue injury and promote tissue repair.

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51
Q

What is the acute phase response driven by? Give three examples

A

Pro-inflammatory mediators. Released by activated macrophages. TNF-alpha, histamine and C3a/C5a

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52
Q

What is the acute phase response mediated by?

A

Hepatocytes, these provide a variety of Acute Phase Proteins.

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53
Q

Examples of Acute Phase Proteins

A
  1. Complement System Proteins: C3 and MBL
  2. C reactive protein
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54
Q

Which cells produce and release cytokines called interferons (IFNα/β)?

A

Virally-infected cells

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55
Q

What do virally infected cells produce and release?

A

IFNα/β

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56
Q

What happens when cells pick up IFNα/β? (3)

A
  1. Signal neighboring uninfected cells to destroy RNA and reduce protein synthesis.
  2. Signals neighboring infected cells to undergo apoptosis
  3. Immune Cells are activated (e.g, NK cells)
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57
Q

What can Natural-killer do?

A

Recognize and destroy virally-infected and cancer cells.

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58
Q

Natural Killer cells attack normal healthy tissues and cells. True or false?

A

False. They ignore those and specifically kill infected cells and abnormal cancer cells.

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59
Q

What is the Complement System

A

It is a heat-labile component of normal plasma that augments the opsonization of bacteria by antibodies and allows antibodies to kill some bacteria.

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60
Q

What does heat-labile stand for?

A

One that is capable of changing or destruction when subjected to heat.

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61
Q

Where can inactive complement system proteins be normally found?

A

Plasma and extracellular fluids

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62
Q

When activated, what cascades of four chemical reactions does the Complement System promotes?

A
  1. Opsonization of pathogens
  2. Direct pathogen killing
  3. Acute inflammation
  4. Leukocyte recruitment
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63
Q

What are the other three plasma cascade systems?

A
  1. THE KININ SYSTEM
  2. THE COAGULATION SYSTEM OR CLOTTING CASCADE
  3. THE FIBRINOLYSIS SYSTEM
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64
Q

What does the Kinin System do?

A

It generates proteins capable of sustaining vasodilation and other physical inflammatory effects

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65
Q

What does the coagulation system do?

A

It forms a protective protein mesh over sites of injury

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66
Q

What does the fibrinolysis system do?

A

It acts in opposition to the coagulation system to counterbalance clotting and generate several other inflammatory mediators

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67
Q

Draw the overview of the Complement System

A

C3 ————–> C3b + C3a (Activation of downstream Complement proteins)
In the arrow, there are:
- Classical Pathway
- Mannose-Binding Lectin Pathway
- Alternative Pathway

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68
Q

Where are the complement proteins synthesized?

A

The liver then pushes it into the circulatory system, where they are inactive.

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69
Q

Describe the Classical Pathway

A
  1. Presence of a pathogen with antigens on its surface.
  2. IgG antibodies bind to these antigens.
  3. Complement proteins bind to the Fc function of the antibody (Order: C1, C4, C2, C3b, C5b, C6, C7, C8, C9)
  4. Proteases activate C3a and C5a.
  5. C3a and C5a are chemotactic agents; they enhance inflammatory response by chemotaxis.
  6. C5b, C6, C7, C8, and C9 can break off and form a MAC (Membrane Attack Complex) attached to the membrane of the bacteria. (H2O and Na+ flow in, and the bacteria undergoes LYSIS)
  7. C3b is an exposed protein and has become an opsonin attracting macrophages
  8. Macrophage’s C3b receptor binds to C3b and engulfs the bacteria.
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70
Q

What does C3 Convertase do?

A

Splits C3 into C3a and C3b

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71
Q

What does C5 convertase do?

A

Split C5 into C5b and C5a

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72
Q

What does MAC stand for?

A

Membrane Attack Complex

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73
Q

What does C3a and C5a do?

A

Enhance inflammatory response by chemotaxis.

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74
Q

Describe the Alternative Pathway

A
  1. C3b is so special it attaches directly to the antigen of the bacteria.
  2. More Complement proteins attach to C3b (C5b, C6, C7, C8, C9)
  3. C3a and C5a are released to enhance inflammatory response.
  4. C5b, C6, C7, C8, and C9 can break off and form a Membrane Attack Complex (MAC).
  5. Bacteria undergo lysis by the flow of H2O and Na+
  6. C3b is exposed, it is an opsonin, and it enhances phagocytosis.
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75
Q

What is there between C3b and C5b, and what does it do?

A

There is factor B/ BB protein and it contributes to the formation of C3/C5 convertases of the alternative complement pathway.

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76
Q

Describe the Mannose-Binding Lectin (MBL)

A
  1. Presence of a pathogen with expressed antigens.
  2. In this case, the antigen is called MANOSE.
  3. There is a protein within our bodies called Manose-Binding Lectin.
  4. Lectin binds to Manose, and the lectin pathway begins.
  5. A protein molecule that likes to bind to MBL is C4.
  6. More proteins bind to C4 (C2, C3b, C5b, C6, C7, C8, C9)
    - proteases activate C3a and C5a to enhance the inflammatory response.
  7. C5b, C6, C7, C8, C9 can break off and for a Membrane Attack Complex.
  8. Bacteria undergo lysis by the flow of H2O and Na+
  9. The C3b is exposed; it is an opsonin. Therefore it enhances phagocytosis.
  10. Phagocyte C3b receptor binds to C3b, and the phagocytes engulf the bacteria.
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77
Q

What can antigens be?

A
  1. Sugar molecules
  2. Protein molecules
  3. Glycoproteins
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78
Q

Who releases proteases?

A

The histamines

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79
Q

What immune system does the Complement System belong to?

A

Innate Immune System, therefore non-specific

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80
Q

What do C3a and C5a do?

A

Enhance inflammatory response by chemotaxis.

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81
Q

What is the difference between all the Complement System Pathways?

A
  • Classical pathway is antibody-mediated
  • Alternative pathway is where C3b directly binds to the antigen.
  • MBL pathway is when Lectin directly binds to mannose (bacteria’s antigen)
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82
Q

Which are the two lymphocytes?

A
  • B cells
  • T cells
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83
Q

What do T cells divide into?

A
  • CD4+ T cells
  • CD8+ T cells
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84
Q

What are B cells responsible for?

A

These are responsible for humoral immune responses. They produce antibodies that attack pathogens circulating the blood and lymph. Plus, their key role is a defense against extracellular pathogens.

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85
Q

What are T cells responsible for?

A

Responsible for cellular immune responses, their key role in defense against intracellular pathogens.

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86
Q

What are CD4+ T cells responsible for?

A

They are the critical regulators of the entire immune system
-Activate B cells (TFH cells)
-Help macrophages (TH1)
-TH2 allergy promotes (IgE)
-T reg– Inactivate lymphocytes to prevent reactions to self-antigens.

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87
Q

What are CD8+ T cells responsible for?

A

They kill virally infected body cells.

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88
Q

What are the two types of recognition?

A

Non-specific and Specific

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89
Q

What is the B cell receptor?

A

An antibody

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90
Q

What are antibodies?

A

Proteins that bind to one specific antigen

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91
Q

What does the structure of an antibody have?

A

The complex of four polypeptide chain
-2x Light chain
-2x Heavy chain

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92
Q

What unique thing do antibodies have, and what does it do?

A

A unique variable region that binds to one specific antigen

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93
Q

Draw the structure of an antibody and label it

A

Check it.

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94
Q

Can antibodies bind to many different types of antigens?

A

Yes

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95
Q

Approximately how many copies of one specific BCR antibody does each B cell express?

A

50,000

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96
Q

What two forms are antibodies expressed in?

A

-Membrane-bound
-Soluble

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97
Q

B cells use membrane-bound antibodies as a receptor to recognize and bind to membrane-associated or soluble antigens. True or false?

A

True

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98
Q

What can the T cells only recognize?

A

They can only recognize peptide antigens

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99
Q

A single T cell expresses just a couple of copies of a single antigen receptor. True or false?

A

False! One can express thousands.

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100
Q

What does each T cell express?

A

A unique T cell antigen receptor that can bind to only one specific peptide antigen.

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101
Q

How do you describe a T cell antigen receptor? (TCR)

A

A membrane-bound protein heterodimer (A dimer made up of two similar but not identical subunits.)

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102
Q

What is a dimer?

A

A molecule or a molecular complex consisting of two identical molecules linked together.

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103
Q

Draw the structure of a TCR and label it

A

α/β TCR chains are the only two things.

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104
Q

What molecules are needed by the T cells to recognize peptide antigens?

A

MHC molecules are needed to present the peptide antigens to the T cells.

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105
Q

What are MHC molecules?

A

Stands for Major Histocompatibility Complex. They are glycoproteins encoded in a large cluster of genes located on chromosome 6

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106
Q

What are MHC molecules also referred to?

A

HLA- Human Leucocyte Antigens.

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107
Q

What is the MHC molecules’ job?

A

Display peptide antigens to T cells; they can present many different ones.

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108
Q

What are the two major classes of MHC molecules?

A
  • Class I MHC
  • Class II MHC
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109
Q

Where are Class I MHC molecules expressed, and do they present peptide antigens to what cells?

A

They are expressed in all nucleated cells
They present peptide antigens to CD8+ T cells

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110
Q

Where are Class II MHC molecules expressed, and do they present peptide antigens to what cells?

A

Expressed only on professional Antigen Presenting Cells (APCs)
-Dendritic cells
-Also, Macrophages, B cells
Present peptide antigen to CD4+ T cells

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111
Q

What does each T cell express?

A

A unique T cell antigen receptor can bind to only one specific peptide antigen.

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112
Q

Where do antigen-specific T cells and B cells develop?

A

In primary lymphoid tissues:
-Bone marrow
-Thymus

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113
Q

Where do adaptive immune responses occur?

A

In secondary lymphoid tissues

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114
Q

What are the secondary lymphoid tissues?

A

Lymph nodes (LNs), spleen, Peyer’s patches (PPs), and mucosal tissues- the nasal-associated lymphoid tissue (NALT), adenoids, and tonsils.

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115
Q

Mature, quiescent, antigen-specific T cells and B cells constantly re-circulate between different blood, secondary lymphoid tissues, and lymphatic vessels. True or false?

A

True.

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116
Q

Where do naïve T Cells and B Cells segregate?

A

Into different areas within secondary lymphoid tissues

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117
Q

How do B cells encounter antigens? Tell me the four steps

A
  1. Dendritic cells phagocytose pathogen-derived particles and antigens
  2. Pro-Inflammatory TNFa stimulates immature tissue-resident Dendritic cells to increase the expression of co-stimulatory molecules.
  3. Dendritic Cells digest ingested proteins and display small peptides derived from these on their cell surface.
  4. Dendritic cells enter the lymphoid tissue and present the antigens.
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118
Q

What two signals do B cells need to receive to become fully activated and clonally proliferate in response to protein antigens?

A
  1. Antigens
  2. Helping signals
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119
Q

What is the germinal center?

A

The germinal center (GC) is a specialized microstructure that forms in secondary lymphoid tissues, producing long-lived antibody-secreting plasma and memory B cells.

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120
Q

What do B cells differentiate into?

A

Plasma cells, to secrete antigen-specific antibodies

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121
Q

Initially, high-affinity antigen-specific IgG antibodies are secreted by short-lived Plasma cells. True or false?

A

FALSE. Initially, low-affinity antigen-specific IgM antibodies are secreted by short-lived Plasma cells.

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122
Q

Later, some B cells mutate to produce and secrete ‘better’ antibodies. Tell me the three steps.

A
  1. Switch from low to high-affinity antibody production. (IgM is the first antibody made against a pathogen. Somatic hypermutation selects for antibodies that bind more tightly to the pathogen)
  2. Switch the class of antibodies that they produce. (Switching antibody isotype to IgG allows delivery of the pathogen to phagocytes)
  3. B cells differentiate into Long-lived Plasma cells and long-lived memory B cells (Bm)
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123
Q

What is Somatic Hypermutation?

A

Somatic hypermutation is a process in which point mutations accumulate in the antibody V-regions of both the heavy and light chains at rates about 106-fold higher than the background mutation rates observed in other genes.

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124
Q

What three elements need to be present for the activation signals to occur?

A
  1. Low-affinity antibodies only
  2. Short-lived plasma cells only
  3. No memory (Bm) cells
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125
Q

What are the two activation signals for Non-protein antigens?

A

Signal 1: BCR + antigen
Signal 2: PRR + PAMP

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126
Q

What are the two activation signals for Antigens With Repetitive Antidenic Epitopes?

A

Signals 1&2: Multiple BCRs + Antigens engaged

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127
Q

What are the two activation signals for Protein Antigens?

A

Signal 1: BCR binding to antigen
Signal 2: Help from TH cells

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128
Q

Describe how antigen-activated B cells undergo clonal expansion and differentiation into antibody-secreting cells (Plasma cells) in secondary lymphoid tissues

A

Protein antigen bound to BCR is internalized by the B cell. The antigen is degraded, and peptides derived from it are presented on the B cell surface in a complex with MHC-II molecules.

Effector TFH cells move into the B cell zone of the lymph node, where they are re-stimulated by B cells in an antigen-specific manner.

Re-activated effector TFH cells stimulate the B cell to clonally proliferate and differentiate into long-lived plasma cells that secrete high-affinity antibodies (Germinal Centre reaction)

Re-activated effector TFH cells stimulate the B cell to clonally proliferate and differentiate into long-lived memory B cells (Bm cells)

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129
Q

What are the two regions of the antibody?

A

Variable region sites and Heavy chain constant region (Fc region)

130
Q

What are the two functions of the antibody?

A

Recognition and Effector function

131
Q

What are the recognition function and the effector function?

A

-Binding to antigen mediated by variable region sites.
-Clearance mechanisms mediated the interaction of the Heavy chain constant region (Fc region) with effector molecules
Complement
Fc receptors

132
Q

What does IgM do in membrane-bound monomeric form and its secreted pentameric form?

A

In membrane-bound monomeric form, IgM serves as the B cell antigen receptor
In its secreted, pentameric form, IgM is the first Ig type produced during a humoral immune response
Present in plasma and secretory fluids
-Agglutination
-Complement system activation

133
Q

What is Agglutination?

A

The action of an antibody when it cross-links multiple antigens producing clumps of antigens.

134
Q

What is agglutination mediated by?

A

Specific antigen binding to IgM and IgG antibodies.

135
Q

What is so good about agglutination?

A

-It increases the efficacy of pathogen elimination by enhancing phagocytosis.
-It prevents viruses from binding to and infecting host cells.

136
Q

What is the Classical pathway activated by?

A
  • Fc region of IgM and IgG antibodies when bound to specific antigens.
137
Q

Which Ig is the most abundant?

A

The most abundant antibody in normal human serum is IgG.

138
Q

When is IgG produced?

A

The dominant Ig type produced during a secondary (memory) immune response

139
Q

What are the six functions of IgG

A

Agglutination
Complement system activation
Foetal immune protection
Neutralisation
Opsonisation
Natural Killer cell activation

140
Q

How does one acquire IgG?

A

IgG antibodies are transported across the placenta directly into the fetal blood circulation

141
Q

What is neutralisation?

A

In the immunological sense, antibodies block the site(s) of bacteria or viruses they use to enter their target cell.

142
Q

What is neutralization mediated by?

A

Specific antigen binding to high-affinity IgG and secretory IgA (sIgA) antibodies

143
Q

IgG are excellent opsonins. True or False?

A

True girl

144
Q

Phagocytes express an Fc receptor that binds specifically to the constant region of the IgG heavy chain. TRUE or FALSE?

A

TRUEEEEEEEEEEEEEEEEE

145
Q

What is Antibody-Dependent Cell-Mediated Cytotoxicity?

A

A type of immune reaction in which a target cell or microbe is coated with antibodies and killed by certain types of white blood cells.

146
Q

What are Natural Killer Cells?

A

An immune cell with granules (small particles) with enzymes that can kill tumor cells or cells infected with a virus.

147
Q

How do you activate Natural killer cells in the innate immune response?

A
  1. Intracellular pathogens infect host cells.
  2. PAMPs are expressed.
  3. The infected host cells secrete interferons (IFN-α, IFN-β)
  4. These interferons activate natural killer cells
  5. They proceed to kill infected host cells and cause the production of pro-inflammatory mediators.
148
Q

How do you activate Natural killer cells in the adaptive immune response?

A

Antigen-bound IgG is another very good activator of Natural Killer cells.
The NK cells bind to the antibody and induce apoptosis in the infected cells.
Then they produce the pro-inflammatory cytokines.

149
Q

What does IgD do?

A

In membrane-bound monomeric form, IgD serves as a B cell antigen receptor
Mediates B cell activation

150
Q

What is the function of IgD in secreted form, and where can it be found?

A

The function of the secreted form of IgD is not well understood.
Found at extremely low concentrations in blood

151
Q

What is the second most abundant Ig type?

A

IgA

152
Q

Where is IgA present, and its function? (In monomeric and secretory form)

A

Present in serum in a monomeric form (IgA)
Functions: Neutralisation

Present in secretory fluids in a dimeric form (secretory IgA, sIgA)
Neonatal defense
Neutralisation (at mucosal sites)

153
Q

How does one get IgA, and why do we need it?

A

IgA antibodies are transported into colostrum and breast milk to protect the GI tract of neonates.

154
Q

What does IgE do?

A

IgE antibodies can trigger allergic responses
-Allergy, asthma, anaphylaxis

155
Q

What class of MHC does CD4+ have?

A

MCH II

156
Q

What class of MHC does CD8+ have?

A

MHC I

157
Q

How are CD4+ and CD8+ T cells activated?

A
  1. Dendritic cells enter the lymph node (T cell zone) and present the pathogen’s antigens.
  2. CD8+ binds with MHC I, and CD4+ binds with MHC II.
158
Q

What is the process of differentiation from Naive CD4+ T cells?

A
  1. Naive CD4+ T cell is presented antigen and co-stimulation.
  2. Undergoes proliferation.
  3. Becomes CD4+ TH0 cells
  4. Then differentiate into CD4+ TH cells (TH1 cells, TH2 cells, TFH cells, Regulatory T cells)
159
Q

What is the function of TH1 cells?

A

TH1 cells migrate out of lymph nodes and enter infected/inflamed tissues to activate macrophages and neutrophils and are critical for host defense against intracellular pathogens such as M. tuberculosis.

160
Q

What pathogens can evade phagolysosomal killing by macrophages?

A

Listeria, Shigella, Mycobacteria, Legionella species.
Infect and propagate in macrophages by escaping from the phagosome into the cytosol

161
Q

What do TH1 T cells do to macrophages?

A

They help them become super-killers.

162
Q

What do TH2 cells do?

A

Th2 cells mediate the activation and maintenance of the humoral, or antibody-mediated, the immune response against extracellular parasites, bacteria, allergens, and toxins. Th2 cells mediate these functions by producing various cytokines such as IL-4, IL-5, IL-6, IL-9, IL-13, and IL-17E (IL-25)

163
Q

What do TFH cells do?

A

T follicular helper cells (Tfh) are a specialized subset of CD4+ T cells first identified in the human tonsil. They play a critical role in protective immunity helping B cells produce antibodies against foreign pathogens.

164
Q

What is the process of differentiation from Naive CD8+ T cells?

A
  1. Naive CD8+ is activated by the presentation of antigens from the dendritic cells.
  2. They undergo proliferation.
  3. They differentiate into killer cells (Cytotoxic T lymphocytes)
  4. These CTLs migrate out of the lymph node and enter sites of infection to kill infected host cells.
165
Q

What is the process of killing by CTLs?

A
  1. CTL recognizes and binds virus-infected cells.
  2. CTL programs target death, inducing DNA fragmentation.
  3. CTL migrates to a new target.
  4. Target cell dies by apoptosis.
166
Q

What are the three proteins in lytic granules of cytotoxic T cells?

A

-Perforin: Polymerizes to form a pore in the target membrane.
-Granzymes: Serine proteases activate apoptosis once in the cytoplasm of the target cell.
-Granulysin: Induces apoptosis.

167
Q

What are cytokines?

A

Cytokines are chemical mediators that regulate cellular immune responses.

168
Q

Draw the GI epithelial barrier (and the cells within it) and label it.

A

A single layer of cells- enterocytes with desmosomes
Apical membrane and basal membrane
Lumen
Crypts of Lieberkühn
Villi and microvilli
M cells
Peyer’s Patch
Lamina Propria
The immune cells- Dendritic cells, B and T cells, and Macrophages.
Other cells: Goblet cells, paneth cells, IE stem cells, enteroendocrine cells, tuft cells, microfold cells.

169
Q

What is the secretory function of the GI epithelial barrier? (Innate immunity)

A

Secrete cytokines, antimicrobial peptides (human defensins, trefoil factors, cathelicidin, REGIIIγ), MUC proteins

170
Q

What is the Gastrointestinal epithelial barrier selectively permeable to?

A

Water, ions, and nutrients.

171
Q

What are the five steps of epithelial barrier growth dynamics?

A
  1. Lgr5+ stem cells in the base of Crypts of Lieberkühn.
  2. Proliferation and differentiation move up the crypt to the villi they shed. (This process takes 3-4 days)
  3. Cell shedding at the tip.
172
Q

What is autophagy?

A

It is your body’s process of reusing old and damaged cell parts.

173
Q

Where are the immune cells located within the GI tract?

A

In the lamina propria.

174
Q

What does the GI mucosal exert?

A

Physiological immunity or tolerance

175
Q

What are Payer’s patches, and what is their function?

A

Peyer’s patches are groupings of lymphoid follicles in the mucus membrane that lines your small intestine. Lymphoid follicles are small organs in your lymphatic system, similar to lymph nodes. Payer’s patches are essential in the immune surveillance of materials within your digestive system.

176
Q

What are M cells and their function?

A

M cells are highly specialized cells within the epithelium overlying organized lymphoid follicles of the small and large intestines. They are central in initiating mucosal immune responses by transporting antigens and microorganisms to the underlying lymphoid tissue.

177
Q

What three tolerances does the GI mucosa develop?

A

Develop Self-tolerance
Non-responsiveness to self-antigens

Develop exogenous tolerance
Non-responsiveness to an enormous array of newly encountered environmental antigens (Food and Microbes)

Develop an effective Immune response Elimination or control of infections, allergic and noxious agents

178
Q

How do microbes impact intestinal epithelial cells (IEC)?

A

IEC sense and respond to microbes

IEC expresses Pattern Recognition Receptors

Stimulate AMP secretion, cytokine responses, TJP regulation – permeability

IEC activity impacts microbial diversity

IEC-produced mucins are energy for microbes.

IEC senses microbial metabolites

E.g., tryptophan catabolites via AhR & PXR – anti-inflammatory, protective in repair

E.g., SCFA – energy source, growth dynamics, permeability

E.g., Bacterial metabolites stimulate serotonin – enteric nervous system and inflammation.

179
Q

How do immune cells impact intestinal epithelial cells and microbiota?

A

Promote barrier repair, eg ILC IL-22

Promote mucin production and AMP secretion eg, ILC derived IL-13 on goblet cells

Macrophage and Treg-derived mediators – stimulate repair

Impact on permeability

180
Q

How do M cells and Dendritic cells work together?

A
  1. M cells take up antigens by endocytosis and phagocytosis.
  2. Antigen is transported across the M cells in vesicles and released at the basal surface.
  3. Antigen is bound by dendritic cells, which activate T cells.
181
Q

What is an interesting characteristic of dendritic cells in the GI mucosa?

A

It can extend processes across the epithelial layer to capture antigens from the lumen of the gut.

182
Q

What is the importance of Dendritic cells in Mucosal immunity?

A

Dendritic cells are important for directing the function of T cells.

183
Q

What are the three signals that determine T-cell response?

A

1) MHC/peptide-TCR
2) CD80-CD28
3) Cytokine

184
Q

Draw the diagram to show the differentiation of Naive T cell and what interleukin each secrete.

A

Check diagram (1) in the notion

185
Q

T cells have an important Role in Maintaining Immune Homeostasis. True or False?

A

True

186
Q

What are the T helper cells and the T regulatory cells which maintain Immune homeostasis?

A

T helper cells: Th1, Th2, Th17
T regulatory cells: Th3, Tr1, Treg

187
Q

What line of defense are macrophages in the gut?

A

The first line of defense

188
Q

What is atopy?

A

The genetic predisposition of an individual to develop allergy disorders.

189
Q

Tell me two functions of the immune system

A

To provide a robust defense against a wide variety of aggressive external agents (mainly microorganisms)
To provide a robust defense against internal aggressive agents (e.g., cancer)

190
Q

What are the two consequences of immune recognition?

A

Intended destruction of the antigen
Collateral tissue damage

191
Q

Define hypersensitivity

A

The immune response that results in bystander damage to the self– an exaggeration of standard immune mechanisms.

192
Q

1

A
193
Q

1

A

1

194
Q

1

A

1

195
Q

What do Th1 cells secrete, and what does it do?

A

IL-2 - They are secreted by them and stimulate growth and differentiation of T cell response.

196
Q

What is the pathophysiology basis of allergy and autoimmunity?

A

Hypersensitivity

197
Q

What is the name of the Classification of hypersensitivity reactions?

A

Gel and Coomb’s classification

198
Q

What are the four types of hypersensitivity reactions? (Number of types and names)

A

Type I: Immediate hypersensitivity
Type II: Direct cell effects
Type III: Immune complex-mediated
Type IV: Delayed type hypersensitivity

199
Q

What are the five immune cells involved in allergies?

A
  1. Mast cells
  2. B-cells
  3. IgE
  4. TH2
  5. Eosinophil
200
Q

What do three things allergic immune responses cause?

A

Cause atopic dermatitis, food allergy, and allergic asthma

201
Q

All adverse reactions are allergic reactions, true or false?

A

False; not all adverse reactions are allergic reactions!!

202
Q

What is the hygiene hypothesis?

A

The hygiene hypothesis proposes that childhood exposure to germs and certain infections helps the immune system develop. This teaches the body to differentiate harmless substances from harmful substances that trigger asthma.

203
Q

What equals a balanced Treg activity?

A

Th1 differentiation stimuli

204
Q

What does a lack of Th1 differentiation stimuli causes?

A

Reduced Treg activity

205
Q

In birth, Th2 is present; what two things could happen?

A
  1. Th1- No allergies
  2. Still Th2– Allergies and asthma
206
Q

What kind of immunity Th1 mediates?

A

Cell-mediated protective immunity

207
Q

What kind of immunity Th2 mediates?

A

Antibody-mediated immunity

208
Q

What are allergic reactions driven by?

A

Driven by TH2 effector cells

209
Q

What three interleukins do TH2 release, and what are they for?

A
  • IL-4 and IL-13: Interact with B cells to cease the production of IgM and initiate IgE production.
  • IL-5: These interact with bone marrow to increase the production of eosinophils- Eosinophilia.
210
Q

What do eosinophils do in immune reactions?

A

Eosinophils mediate allergic and asthmatic symptoms.

211
Q

What are the five steps of how the allergen is cleared in immune reactions?

A

-Mast cells and basophils express receptors that bind to theFc region of IgE antibodies on their surface (Fce receptors)
-On the first encounter with an allergen, B cells produce antigen-specific IgE antibody
-Allergen is cleared
-Residual IgE antibodies bind to mast cells/basophils via Fc receptors.
-No great consequence initially

212
Q

What is the sensitization stage?

A

A sensitization phase in which unprimed or memory T cells interact with dendritic cells to become active lymphoblasts

213
Q

What is the pathological stage?

A

Allergy is established, and great consequences come when re-encountered with an allergen.

214
Q

What are the three things that happen when the allergen is re-encountered?

A

Allergen binds to IgE-coated mast cells, &basophils– degranulation
Release of vasoactive mediators (histamine, tryptase)
Also, increased expression of pro-inflammatory cytokines and leukotrienes

215
Q

What do T-regulatory cells do?

A

They are responsible for the inactivation of lymphocytes, so they do not cause reactions against self-antigens.

216
Q

Why are asthmatics sensitive to aspirin?

A

Immune cells confuse it with pathogens and initiate an allergic response.

217
Q

What are the seven specific allergy features?

A

Asthma
Urticaria- a raised, itchy rash that appears on the skin.
Angioedema
Allergic rhinitis (hayfever)
Allergic conjunctivitis
Diarrhea and vomiting
Anaphylaxis

218
Q

What is the time of reaction when exposed to an allergen?

A

Occurs quickly after exposure to an allergen (minutes – 1-2 hours)

219
Q

How can one manage IgE-mediated allergic disorders? (7)

A

Avoidance of allergen
Block mast cell activation
Prevent effects of mast cell activation
-Anti-histamines
-Leukotriene receptor antagonists
Anti-inflammatory agents
Adrenaline
Immunotherapy

220
Q

What antibody are allergies mediated by?

A

IgE

221
Q

Allergues are mediated by IgE antibody together with mast cells, what can this also give rise to?

A

Eosinophil recruitment and activation

222
Q

Antigens that can trigger these reactions are known as….

A

Allergens

223
Q

People, who suffer unduly from allergies have usually high levels of what? And what are these people called?

A

People who suffer unduly from allergy usually have raised levels of IgE in their blood and are called ‘atopic’

224
Q

What number of genes are usually involved in inherited allergies?

A

At least 12 genes

225
Q

Mast cell degranulation can also be triggered directly by tissue injury and complement activation and by some bacteria independently of IgE. True or false?

A

True!

226
Q

Tell me the five steps of an IgE-mediated antibody response to an external antigen’s pathophysiology.

A

-Production of specific IgE directed against an allergen (B cells, TFH cells, TH2 cells)
-Allergen-specific IgE binds to mast cells via Fc receptors
-Re-exposure to the allergen results in its binding to the mast cell-bound IgE, resulting in activation and degranulation of the mast cell
-Release of pre-formed and newly synthesized inflammatory molecules, e.g., histamine and leukotrienes
-These mediate the local and systemic effects of the allergic reaction

227
Q

What is Type 1 Hypersensitivity mediated by?

A

IgE-Mediated Hypersensitivity.

228
Q

What is Type II mediated by?

A

IgG- or IgM-Mediated Cytotoxic Hypersensitivity

229
Q

What is type III Hypersensitivity mediated by?

A

Immune-Complex mediated Hypersensitivity

230
Q

What is type IV Hypersensitivity mediated and driven by?

A

Cell-Mediated Hypersensitivity, driven by CD4+

231
Q

What happens in Type I hypersensitivity?

A

Antigen induces cross-linking of IgE bound to mast cells and basophils by releasing vasoactive mediators.

232
Q

What happens in Type II hypersensitivity?

A

Antibodies directed against cell surface antigens mediate cell destruction via complement activation or ADCC.

233
Q

What does ADCC stand for?

A

Antibody-dependent cell-mediated cytotoxicity

234
Q

What happens in Type III Hypersensitivity?

A

Antigen-Antibody complexes deposited in various tissues induce complement activation and an ensuing inflammatory response mediated by massive infiltration of neutrophils.

235
Q

What happens in Type IV Hypersensitivity?

A

Sensitized TH1 cells release cytokines that activate macrophages or Tc cells that mediate direct cellular damage.
TH2 cells and CTLs (Cytotoxic T lymphocytes) mediate similar responses.

236
Q

What are the two typical manifestations of Type I Hypersensitivity?

A

-Systemic Anaphylaxis
-Localized Anaphylaxis

237
Q

What are the three typical manifestations of Type II Hypersensitivity?

A

-Blood transfusion reactions
-Erythroblastosis fetalis
-Autoimmune hemolytic anemia.

238
Q

What are the two typical manifestations of Type III Hypersensitivity?

A
  • Localized Arthus reaction
    -Generalized reactions, such as Rheumatoid arthritis and systemic lupus erythematosus.
239
Q

What are the three typical manifestations of Type IV Hypersensitivity?

A

-Dermatitis
-Tubercular lesions
-Graft rejection

240
Q

What are Type IV hypersensitivity reactions also known as?

A

delayed-type hypersensitivity

241
Q

What are the three classical hallmarks of a type IV reaction?

A

-A large number of macrophages at the reaction site
-That it takes an average of 24-48 hrs for symptoms to manifest after re-exposure to the initiating antigen
-Granulomas often form due to infectious pathogens/foreign bodies that cannot be cleared.

242
Q

What are the four steps in the effector phase (Local tissues)

A

-Reactivation of TH1 cells by antigen-presenting macrophages
-Release of pro-inflammatory cytokines by TH1 cells
-Activation of macrophages
-Tissue damage and destruction

243
Q

Define Autoimmunity

A

The presence of immune responses against self-antigens.

244
Q

What is the harmful aspect of autoimmunity?

A

High titers of auto-antibodies or auto-reactive T cells. Which causes significant tissue/organ damage and chronic inflammation.

245
Q

What connects the light chain and heavy chain of antibodies?

A

Disulfide bridge

246
Q

Name the four steps of B cell development

A
  1. Stem cells
  2. Lymphoid progenitors
  3. Progenitor B cell
  4. Mature B cell IgM (B cell receptor)
247
Q

How are antibodies generated?

A

Generated by the production of the heavy chain (HC) and light chain (LC) polypeptides that are synthesized from two separate immunoglobulins (Ig) genes

248
Q

What are the Heavy chain Ig and the Light chain Ig composed of?

A

Segmented Genes- VDJ recombination

249
Q

Is antigen receptor gene rearrangement in developing T and B cells planned or random?

A

Random

250
Q

How does the immune system deal with autoreactive T cells and B cells?

A

-Specific ‘tolerance’ mechanisms are used to kill or inactive auto-reactive lymphocytes:

-Deletion of self-reactive lymphocytes in primary lymphoid tissues (central tolerance)

-Regulatory T cells (TREG cells) can help inactivate auto-reactive lymphocytes in peripheral tissues that escape central tolerance (peripheral tolerance)

251
Q

What is a T-reg cell for?

A

Inactivation of lymphocytes.

252
Q

What is T-reg crucial for?

A

Suppressing hyper-reactive or auto-reactive T cells via the production of anti-inflammatory cytokines.

253
Q

Describe the pathogenesis of autoimmune diseases

A
  1. Have a genetic susceptibility.
  2. Breakdown of immune tolerance to self-antigens (Loss of immune regulation  generation/activation of autoreactive B and T cells)
  3. Two things can happen, autoimmune phenomena and autoimmune disease.
254
Q

What are Monogenic disorders?

A

Single gene defects that cause autoimmune diseases. These are rare

255
Q

Example of a monogenic disorder

A

IPEX Syndrome- A genetic disease of immune dysregulation that causes diarrhea, diabetes, and eczema in young patients.

256
Q

Five symptoms of IPEX Syndrome

A

Severe infections
Intractable diarrhea
Eczema
Very early onset insulin-dependent diabetes mellitus
Autoimmune manifestations

257
Q

What are the two treatments (There is a cure) for IPEX syndrome?

A

-Cure: hematopoietic stem cell transplantation (HSCT)
-Supportive care: immunosuppressive drugs plus total parenteral nutrition

258
Q

What does IPEX stand for?

A

Immune dysregulation, Polyendocrinopathy, Enteropathy, and X-linked inheritance syndrome

259
Q

What is the pathogenesis of IPEX syndrome?

A

-Condition is X-linked

-Caused by mutations in the FOXP3 gene

-Hence, IPEX causes a failure of peripheral tolerance mechanisms due to the absence of regulatory T cells

260
Q

What do most autoimmune diseases result?

A

From complex genetic interplay (HLA genes- Remember it is the same as MHC)
-Genes determining sex
-Other immune response genes

261
Q

How many MCH-I are on all nucleated cells and from what are the derived?

A

Six Class I molecules (three maternally derived, three paternally derived)

262
Q

What are the molecules (HLA) called in all nucleated cells called?

A

HLA-A, HLA-B and HLA-C

263
Q

How many MCH-II are on specialized antigen-presenting cells, and from what are they derived?

A

Six MCH-II molecules (three maternally derived, three paternally derived)

264
Q

What are the molecules (HLA) in all specialized antigen-presenting cells called?

A

HLA-DR, HLA-DQ and HLA-DP

265
Q

All HLA genes are highly polymorphic. True or false?

A

True

Polymorphism, as related to genomics, refers to the presence of two or more variant forms of a specific DNA sequence that can occur among individuals or populations.

266
Q

What is two sex bias in certain autoimmune diseases?

A
  1. Sex hormones are known to influence lymphocyte function in males versus females
  2. Alterations in disease severity for some autoimmune diseases are known to occur during pregnancy
267
Q

What four environmental factors can trigger autoimmunity in genetically predisposed individuals?

A

Infections
Cigarette smoking
Hormone levels
Tissue damage

268
Q

What mechanism factors can trigger autoimmunity in genetically predisposed individuals?

A

Molecular mimicry
Alterations to self-antigens
Antigen sequestration
Bacterial superantigens

269
Q

What is Acute rheumatic fever after Group A Streptococcal infection an example of?

A

Molecular mimicry.

270
Q

Why does the Strep. M5 protein cause rheumatic fever?

A

Because the streptococcal cell wall stimulates antibody response and some antibodies cross-react with heart tissue, causing rheumatic fever.

271
Q

What is Drug-induced hemolytic anemia?

A

A blood disorder occurs when a medicine triggers the body’s defense (immune) system to attack its red blood cells.

272
Q

What drug can cause drug-induced hemolytic anemia, and what is it used for?

A

Ceftriaxone is used to treat bacterial infections in many different body parts.

273
Q

What is post-traumatic autoimmune uveitis

A

An inflammatory reaction of the uvea and iris, typically developing within three days of blunt eye trauma.

274
Q

Bacterial toxins can act as ______. These can ____ activate all _____, including ___ and __ cells.

A

Superantigens. Lymphocytes. T and B

275
Q

What are the two classifications for autoimmune diseases?

A
  1. Clinical classification
    Organ-specific diseases
    Non-organ specific or multisystem autoimmune diseases
  2. Pathological classification
    Gel and Coombs classification
276
Q

What six autoimmune diseases are driven by type II hypersensitivity reactions?

A

Blood cells - Autoimmune hemolytic anaemia
Endocrine system - Graves’ disease
Kidney/Lung - Goodpasture’s syndrome
Nervous system - Guillan Barre syndrome
Musculoskeletal system - Myasthenia Gravis
Skin - Pemphigus vulgaris

277
Q

Tell me, what does Grave’s disease cause, how does it cause it, and what is the mechanism?

A

A leading cause ofhyperthyroidism

Auto-antibodies have generated that bind to the thyroid-stimulating hormone receptor (TSHR)

Mechanism = type IIb hypersensitivity reaction
Antibody binding to the TSHR stimulates the receptor-increased T3 and T4 secretion.

278
Q

Tell me what is Goodpasture’s syndrome, what it affects, what it can cause, its symptoms, and what treatment

A

-An autoimmune disease that affects the lungs and kidneys
Pulmonary alveolar hemorrhage
Kidney disease (glomerulonephritis)
-Symptoms:
Hemoptysis, dyspnea, fatigue, chest pain, and/or anemia.
-Treatment:
Immunosuppressive drugs
Anti-inflammatory drugs
Plasmapheresis
Stop smoking!

279
Q

What is Goodpasture’s Syndrome defined by?

A

The presence of autoreactive antibodies to the α3 chain of type IV collagen present in the basement membranes of alveoli and glomeruli

280
Q

What three autoimmune diseases are driven by type III hypersensitivity reactions?

A

-Systemic lupus erythematosus (SLE)
-Rheumatoid arthritis (secondary to disease driven by type IV reactions)
-Glomerulonephritis (some types)

281
Q

Tell me what is Systemic Lupus Erythematous, its symptoms, the peak age of onset, who is more likely to get it, and how you get it.

A

It is a rare prototypic multi-system autoimmune disease.
-Symptoms:
Fatigue.
Fever.
Joint pain, stiffness, and swelling.
A butterfly-shaped rash on the face that covers the cheeks and bridge of the nose or rashes elsewhere on the body.
Skin lesions that appear or worsen with sun exposure.
Fingers and toes that turn white or blue when exposed to cold or during stressful periods.
-Peak age: 2nd or 3rd decades, and high female preponderance (90% of cases)
-STRONG genetic predisposition.

282
Q

What happens at the cellular levels in SLE?

A

Increased apoptosis, defective clearance of apoptotic material and immune complexes, and dysregulation of neutrophil NETs promote type III hypersensitivity reactions in SLE.

283
Q

What infections are the major hallmark of immune deficiency?

A

Recurrent

284
Q

Explain SPUR infections

A

Serious infections
-Unresponsive to oral antibiotics
Persistent infections
-Early structural damage
-Chronic infections
Unusual infections
-Unusual organisms
-Unusual sites
Recurrent infections
Two major or one major and recurrent minor infections in one year

285
Q

Other six features that may be suggestive of primary immune deficiency

A

Weight loss, family history, cancer, chronic diarrhea, mouth ulcers, skin rash, and other autoimmune disorders

286
Q

What are primary and secondary autoimmune disorders?

A

Primary are rare genetic disorders that impair the immune system.
Secondary disorders develop due to an existing pathological process.

287
Q

Five conditions associated with secondary immune deficiency

A
  1. Physiological immune deficiency
  2. Infection
  3. Treatment interventions
  4. Malignancy
  5. Biochemical and nutritional disorders
288
Q

What are the primary and initial manifestations in most cases and the most common complication in primary immunodeficiency disorders?

A

Respiratory diseases

289
Q

What are the upper respiratory complications?

A
  1. Sinusitis
  2. Otitis Media
  3. Laryngeal Angioedema
290
Q

What are the lower respiratory complications?

A
  1. Malignancies
  2. Interstitial Lung Diseases
  3. Pneumonia
  4. Bronchitis and Bronchiectasis
291
Q

What is Kostmann Syndrome, what types is the most common, what does it cause, clinical manifestations and treatment?

A

A rare genetic disorder, SCN type I is the most typical form and is inherited in an autosomal dominant manner. Caused by mutations in the ELANE gene on chromosome 19p13.3, which encodes for neutrophil elastase
- Clinical manifestations
Severe chronic neutropenia from birth
Absolute neutrophil count <200/μL (normal >3000/μL)
Accumulation of precursor cells in the bone marrow
Recurrent bacterial/fungal infections (no pus)
Within two weeks of birth
-Treatment: recombinant G-CSF
Reduces infections and improves survival
Increased risk of AML or myelodysplasia

292
Q

What would you expect to happen if a patient’s phagocytes could not bind to endothelial adhesion molecules?

A

Failure to recognize activation markers expressed on endothelial cells
Neutrophils are mobilized but cannot exit the bloodstream

293
Q

What is Endothelial Adhesion Marker Dysfunction, what is it caused by, what does it result in, and what are the clinical picture characteristics and the treatment?

A

Very rare autosomal recessive primary immunodeficiency
Caused by a genetic defect in the CD18 integrin gene
Results in failure of neutrophil adhesion and migration
The clinical picture is characterized by marked leukocytosis and localized bacterial infections
The treatment is hematopoietic stem cell transplantation.

294
Q

What is Chronic Granulomatous Disease, the most typical form, and what effect does it have on the body? Lastly, at what age does it present?

A

Deficiency of the intracellular killing mechanism of phagocytes - absent respiratory burst
The most typical form is a deficiency of the p47phox gene – a component of the NADPH oxidase complex (X-linked inheritance)
Inability to generate oxygen/nitrogen free radicals (ROS/RNS)
The impaired killing of intracellular micro-organisms.

-It is usually diagnosed before the age of 5, and is characterised by recurrent infections by pus-forming (pyogenic) bacteria, especially Staphylococcus aureus.

295
Q

What is the three treatments for Chronic Granulomatous Disease?

A

-Immunoglobulin replacement therapy (IVIg)

-Aggressive management of infection
Oral/intravenous antibiotics and anti-fungals
prophylactic use may be indicated
Surgical draining of abscesses

-Definitive therapy
Haematopoietic stem cell transplantation
Specific treatments:
SCN – recombinant G-CSF
Gene therapy

296
Q

What are the five clinical features of CGD?

A

-Recurrent deep bacterial infections
-Especially Staphylococcus, Aspergillus, pseudomonas cepacia
-Mycobacteria, atypical mycobacteria
-Recurrent fungal infections
-Failure to thrive
-Lymphadenopathy and hepatosplenomegaly
-Granuloma formation

297
Q

What is Severe Combined Immunodeficiency?

A

Failure of production of lymphocytes

298
Q

Causes of SCID

A

->20 possible pathways identified
Deficiency of cytokine receptors
Deficiency of signalling molecules
Metabolic defects
Defective receptor rearrangements

-Presence of different lymphocyte subsets (T, B, NK) depend on exact mutation

299
Q

What is the commonest form of severe combined immunodeficiency?What is the clinical phenotype? What age does it present?

A

-X-linked SCID is the most common.
- Mutation of a component of the IL-2 Receptor. (Shared by many other cytokine receptors. Results in inability to respond to cytokines
failure of T cell and NK cell development. Production of immature B cells)
Clinical phenotype:
-Very low or absent T cells; because IL2 is so important for T cell development
Normal or increased B cells
Poorly developed lymphoid tissue and thymus

-It usually presents at 6 months of age with recurrent severe bacterial, fungal and viral infections.

300
Q

What are the six clinical phenotype in SCID patients?

A

-Unwell by 3 months of age
-Persistent diarrhoea
-Failure to thrive
-Infections of all types
Common infections – more severe than usual
Unusual & opportunistic infections
Vaccine associated diseases
-Unusual skin disease
-Graft versus host disease
-Colonisation of infant’s “empty” bone marrow by maternal lymphocytes
-Family history of early infant death

301
Q

What is the treatment for SCID?

A

-Prophylactic treatment
Avoid infections
Prophylactic antibiotics
Prophylactic antifungals
No live attenuated vaccines
Aggressive treatment of existing infections
Antibody replacement - Intravenous immunoglobulin
- Definitive treatment
Stem cell transplant from HLA identical sibling if possible
Stem cell transplant from other sibling or parent, or from matched unrelated donor

302
Q

What are the eight symptoms of Bruton’s X-linked hypogammaglobulinaemia?

A

Bronchitis (airway infection)
Chronic diarrhea.
Conjunctivitis (eye infection)
Otitis media (middle ear infection)
Pneumonia (lung infection)
Sinusitis (sinus infection)
Skin infections.
Upper respiratory tract infections.

303
Q

What is Bruton’s X-linked hypogammaglobulinemia, and at what age does it present?

A

No circulating B cells
No plasma cells
No circulating antibody after the first 6 months

BTK* gene is essential for B cell development
(* Bruton’s Tryosine Kinase)

-It presents at 6-9 months of age with recurrent severe episodes of pneumonia, upper respiratory tract infections, and gastrointestinal infections. Skin and joint infections are also common.

304
Q

What interleukin and interferon is activated to fight infections with mycobacteria?

A

IL-12: IFNɣ network

305
Q

What are the four steps of the mechanism which fights infection with mycobacteria?

A
  1. Infected macrophages produce IL-12
  2. IL-12 stimulates NK cells and TH1 cells to secrete IFN
  3. IFN-gamma feeds back to macrophages and neutrophils
  4. Stimulates production of TNF-alpha, and activates NADPH oxidase complex.
306
Q

What cells mediate acute and chronic organ rejection? (Days to weeks)

A

Helper T cells.

307
Q

What cell mainly secretes Interferon-gamma?

A

Th1 cells

308
Q

What is selective immunoglobulin A deficiency?

A

This is usually asymptomatic (90-95% of cases). When symptoms do occur, they can present at any age. It is characterized by infections of the respiratory and gastrointestinal tracts, as IgA usually provides localized protection on mucous membranes.

309
Q

What is Wiskott-Aldrich Syndrome, what does it lead to, and what is characterized by?

A

Wiskott-Aldrich syndrome causes impaired T-cell function. This leads to recurrent viral, bacterial, and fungal infections within the first year of life. It is also characterized by low platelets (thrombocytopenia), which causes marked bruising and mucosal bleeding (especially nosebleeds).

310
Q

What cells mediate hyperacute organ rejection?

A

B cells

311
Q

What immunoglobulin can transfer to her baby?

A

IgG

312
Q

Which primary lymphoid area, active in the 4-month-old, is where T cells undergo primary development?

A

The thymus

313
Q

Which cytokine is primarily responsible for activating macrophages?

A

Interferon-gamma

314
Q

What are the four clinical features of inflammatory process?

A

Rubor, calor, tumor and dolor

315
Q

The inflammatory cell that characterizes acute inflammation

A

Neutrophils

316
Q

CD4+ differentiate into Th2, and these act on B cells to form…

A

IgE

317
Q

Why IgM to IgG?

A

Way more cells have IgG receptors

318
Q

What is Immunoglobin switching modulated by?

A

Cytokinesssss

319
Q

What are the differences between Plasma Cells and B memory cells?

A
320
Q

Memory response vs. naive response, why is memory response better?

A

Foundations of Medicine (18 decks)

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