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Med Year 1 - IMS > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the immune system?

A

A complex group of molecules, cells, tissues and organs that provide protection from microbes, tumour cells and foreign material.

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2
Q

What are 5 types of microbes and their examples?

A
  • Bacteria (MRSA)
  • Viruses (COVID)
  • Protozoa (malaria)
  • Helminths (pinworm)
  • Fungi (candida)
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3
Q

What is an antigen?

A

A substance that when recognised by the immune system, will trigger an immune response

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4
Q

What are examples of an antigen?

A
  • pollen
  • proteins in peanuts
  • proteins on surface of viruses
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5
Q

How can an antigen normally be recognised?

A

Often can only be recognised by the immune system if ‘presented’ on the surface of an antigen presenting cell (APC)

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6
Q

What is the basic format of an APC?

A

antigen at the top, connected to MHC (major histocompatibility complex) or HLA (human leukocyte antigen complex. This is connected to the APC.

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7
Q

What is an antibody?

A

An immunoglobulin (Ig). It is a specific protein made in response to an antigen and is produced by B cells.

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8
Q

What does a neutrophil do?

*bi-lobed nucleus

A
  • Rapidly enters the infected tissues in large numbers and release toxic chemicals (e.g MPO), release chemicals to attract other immune cells (cytokines), phagocytose organisms and create neutrophil extracellular traps (NETs)
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9
Q

In which microbe infection are neutrophils particularly useful in? And what does it form?

A
  • Bacterial/ fungal infections
  • Forms pus (dead neutrophils)
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10
Q

What are the three types of neutrophil immune response?

A
  • degranulation
  • phagocytosis
  • NETosis
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11
Q

What is the difference between basophils and mast cells?

A
  • Basophils are found circulating in the blood
  • Mast cells are found in the tissues
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12
Q

What are similarities between basophils and mast cell function?

A
  • Both release histamine (a vasodilator)
  • This helps in the defence against multicellular parasites e.g. helminths
  • can cause tissue damage in allergy
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13
Q

What do eosinophils contain which help in immune defence? What can happen during an allergy?

A
  • Contain red granules containing toxic proteins and free radicals
  • These help in the defence against multicellular parasites e.g. helminths
  • Can cause tissue damage in allergy (esp asthma)
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14
Q

Where are dendritic cells located?

A

Located in tissues that are common points for initial infection such as the skin, lungs and GI tract.

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15
Q

What is the main role of a dendritic cell?

A
  • Main role is as an APC
  • They migrate to lymph nodes, antigen present to other cells and activate a specific immune response
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16
Q

What is the difference between monocytes and macrophages?

A
  • Monocytes are found circulating in the blood
  • Macrophages are found in the tissues
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17
Q

What is the function of monocytes and macrophages?

A
  • Phagocytosis of debris/dying cells/ microbes
  • APC (migrate to lymph nodes, antigen present to other cells = activation of specific immune response)
  • Recruit other immune cells (cytokines)
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18
Q

What do natural killer cells do?

A
  • release perforins and granzymes
  • Trigger apoptosis in infected host cells (i.e. do not attack the pathogen directly)
  • Trigger apoptosis in cancerous cells
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19
Q

What two types of (small) lymphocytes are there?

A
  • T-lymphocyte (T-cell)
  • B-lymphocyte (B-cell)

*Have very little cytoplasm

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20
Q

What is a plasma cell?

A

A specialised type of B cell which makes antibodies

*Have much more cytoplasm to make more organelles

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21
Q

What happens in the primary lymphoid tissue and what are examples?

A
  • This is where lymphocytes develop and mature
  • Bone marrow
  • Thymus gland
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22
Q

What happen in the secondary lymphoid tissue

A
  • This is where lymphocytes encounter antigens/pathogens
  • It includes the lymph nodes, spleen and lymph-oid tissues at other sites e.g. tonsils, adenoids, Peyer’s patches
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23
Q

Where is bone marrow found?

A

In the centre of large bones

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24
Q

What is bone marrow the site of production of?

A
  • white blood cells
  • red blood cells
  • platelets
  • It is also the site of B cell maturation
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25
Q

What is the thymus the site of?

A

T-cell maturation (T-cells are produced in the bone marrow first)

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26
Q

Where is the thymus found and what is the difference in adults compared to children?

A
  • Gland behind the sternum
  • It is larger in children and small and fatty in adults
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27
Q

Where are lymph nodes found?

A
  • Throughout the body
  • Large numbers in the neck, axilla, groin and paraaortic area etc
  • Connected via channels of lymphatic vessels
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28
Q

What is the function lymph nodes?

A
  • Act as areas to ‘filter out’ any infection or cancer cells from the lymph fluid
  • APCs in the lymph fluid can meet many naïve B and T cells in a lymph node
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29
Q

Where is the spleen found?

A

Organ in the upper outer quadrant of the abdomen

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30
Q

What are the two tissues that are mixed in the spleen?

A
  • White pulp
  • Red pulp
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31
Q

What does white pulp do?

A

Lymphocytes are stimulated by antigens (i.e. just like a lymph node)

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32
Q

What does the red pulp do?

A

Filters out old red blood cells

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33
Q

What are the ways of classifying types of immunity?

A
  • Innate immunity v adaptive/acquired immunity
  • Humoral immunity v cell mediated immunity
  • Passive immunity v active immunity
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34
Q

What are the characteristics of innate immunity?

A
  • ‘First line’
  • Rapid
  • Short lasting
  • Non-specific

The innate immune system triggers the adaptive immune system by presenting antigens.

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35
Q

What are characteristics of adaptive/ acquired immunity?

A
  • ‘Second line’
  • slow
  • Long lasting
  • specific (to the antigen)
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36
Q

What are mechanical/physical barriers for innate immunity?

A
  • Intact skin and mucous membranes
  • Mucus and cilia
  • Tears and eyelashes
  • Sweat and body hair
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37
Q

What are chemical mediators of innate immunity?

A
  • lysozyme (cleaves bacterial cell wall)
  • Interferon (induces antiviral defences in uninfected cells)
  • Complement (lyses microbes/facilitates phagocytosis)
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38
Q

Immune cells involved in the innate response?

A
  • Phagocytes (macrophages and neutrophils)
  • Mast cells
  • Monocytes
  • Dendritic cells
  • Natural killer (NK) cells (triggers apoptosis of infected cells)
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39
Q

What are some conditions or effects of innate immunity?

A
  • Competition by normal bacterial flora
  • Stomach acid pH
  • Fever (inhibits pathogen growth)
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40
Q

What two immune cells does adaptive immunity utilise?

A
  • B-lymphocytes (and the specific antibodies they produce)
  • T-lymphocytes
  • Macrophages
  • dendritic cells
  • NK cells
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41
Q

What is the difference between humoral vs cell mediated immunity (sub-divisions of adaptive immunity)

A
  • Humoral uses B-lymphocytes
  • cell mediated immunity uses T-lymphocytes
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42
Q

What is passive immunity?

A

You receive antibodies somebody else made
- Naturally eg from mother to foetus via placenta/breast milk
- Artificially eg post exposure prophylaxis immunoglobulin injections for certain infection.
- Short term protection

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43
Q

What is active immunity?

A
  • You make your own antibodies/mount your own immune response
  • long term protection
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44
Q

When does the innate immune response occur compared to the adaptive immune response?

A

Innate immunity occurs within the first few days and adaptive immunity develops from around a week.

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45
Q

Why is the innate immune system known as ‘innate’?

A
  • since all animals have the system
  • evolutionarily the oldest natural defence against infection
  • first line of attack to deal with pathogens before the adaptive immune system kicks in
  • Produces local redness and swelling associated with infections
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46
Q

What are the three stages of the innate response?

A

Responds to invading pathogens immediately upon contact

Involves humoral and cellular responses
- complement activation (blood plasma)
-phagocytosis by macrophages and neutrophils
- NK cells

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47
Q

Does the innate immune system have a memory system?

A

Adaptive immune system produces a faster, more efficient response with the same pathogens, the innate immune system responds in the same way every time to repeated infection

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48
Q

Which part of the innate immune system involves the complement system and which phase involves macrophages, dendritic cells, neutrophils and NK cells?

A

complement system = humoral phase
macrophages, dendritic cells, neutrophils, NK cells = cellular phase

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49
Q

what are the effectors of the complement cascade system?

A
  • MAC
  • Anaphylatoxins
  • Opsonisation
  • Neutrophils are attracted to the site of the infection
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50
Q

What is the MAC?

A

Membrane attack complex of several complement factors that perforates ‘stabs’ the cell membrane of a pathogen or a virus infected cell.

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51
Q

What are anaphylatoxins?

A

Byproducts from activated complement factors which play a role in allergic reactions and anaphylactic shock

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52
Q

What are the 3 complement activation pathways?

A
  • Classical
  • Lectin or mannose-binding
  • Alternative
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53
Q

Which complement factors are all 3 complement activation pathways centred around?

A

Complement factors C3 and C5

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54
Q

What is the classical pathway activated by?

A

Activated by antigen-antibody complexes (so adaptive immune system has to be activated)

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55
Q

What are many of the complement factors for the classical pathway and and what does their activation involve?

A
  • Many of the complement factors are serine proteases
  • Similar to blood coagulation, complement activation involves limited proteolysis to activate the next factor.
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56
Q

What does the classical pathway produce?

A

Produces anaphylatoxins, opsonins and MAC

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57
Q

What is limited proteolysis?

A

They cleave only one (or few) other protein(s) in only one place which leads to the activated complement factor and a byproduct

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58
Q

Which complement factor activates the classical component pathway? And what does it bind to?

A

Complement factor C1 binds to antibody/antigen complexes (generated by the adaptive immune system)

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59
Q

What are the five steps of the classical pathway?

A

1) C1 cleaves complement factor C2 into C2a and C2b
2) C1 also cleaves factor C4 into C4a and C4b
3) C2a and C4b form a complex which cleaves factor C3 into C3a and C3b
4) C3b joins the C2a/C4b complex forming a C2a/C4b/C3b complex which cleaves C5 into C5a and C5b
5) C5b forms a complex with C6, C7, C8, C9 producing the membrane attack complex (MAC) which perforates the pathogen cell membrane or virus-infected host cells.

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60
Q

What are some of the byproducts of the classical pathway that play a role in anaphylaxis and opsonisation?

A
  • C3a, C4a and C5a are anaphylatoxins
  • C3b plays a role in opsonisation
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61
Q

What does the mannose-binding lectin (MBL) pathway do?

A

Binds mannose (sugar) found on the surface of pathogens, binds MBL Associated Serine Protease (MASP) 1 and 2 which activates (cleaves) C2 and C4.

*Rest of the pathway (C3-9) is identical to the classical pathway

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62
Q

What is the lectin complement pathway activated by?

A

Directly activated by pathogens (first pathway to be triggered)

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63
Q

Where is mannose found on the cell?

A

On the cell membrane/envelope of many pathogens but not on the host cells

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64
Q

What are some examples of pathogens that activate the Lectin pathway?

A
  • Yeast (Candida albicans)
  • Viruses (HIV and influenza A)
  • Bacteria (Salmonella and Streptococci)
  • Parasites (Leishmania)
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65
Q

What are the steps in the Alternative pathway?

A

Activated by direct contact with pathogens

  • Complement factor C3 undergoes spontaneous slow rate auto-activation of C3 (producing C3b).
  • Low levels of C3b bind to the bacterial membrane
  • Two other proteins, factor B and properdin bind to C3 on the bacterial surface, which rapidly activates more C3 and activates C5.
  • Rest of pathway is same as the classical pathway (C6-9)
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66
Q

What do anaphylatoxins (C3a, C4a and C5a) do?

A
  • They trigger the degranulation of endothelial cells, mast cells (histamine) and phagocytes
  • Cause vasoconstriction through smooth muscle contraction and enhance vascular permeability
  • C3a and C5a are chemoattractants for neutrophils
  • Involved in allergic reactions but in large quantities they may cause anaphylactic shock
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67
Q

What does the degranulation of phagocytes release?

A

Release cytokines

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68
Q

What does enhanced vascular permeability by anaphylatoxins allow for?

A

Make the blood vessel walls ‘leaky’ making it easier for neutrophils and natural killer cells to infiltrate infected tissue.

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69
Q

What is opsonisation?

A

Process whereby pathogens are labelled to increase recognition of the pathogens by phagocytes

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70
Q

What is the process of opsonisation by C3b?

A
  • C3b binds to the pathogen
  • C3b is cleaved to iC3b
  • iC3b is recognised by receptors on the macrophage cell membrane, enhancing phagocytosis
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71
Q

Which three cells have phagocytosis as their main function?

A
  • macrophages
  • dendritic cells
  • neutrophils
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72
Q

What is the pathway for phagocytosis?

A
  • Pathogens are engulfed by the (macrophage, dendritic cell or neutrophil) cell membrane forming phagosomes
  • The phagosome fuses with a lysosome that contains digestive enzymes and forms a phagolysosome
  • The digestive enzymes in the phagolysosome digest the pathogen
  • Formation of the residual body which contains indigestible material
  • Secretion of waste materials out of the cell by fusion of the residual body with the cell membrane.
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73
Q

Where are macrophages located in the body?

A

skins, lungs and intestines

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74
Q

What are three main activation states of macrophages?

A

Resting, primed and hyper-active

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75
Q

What does the resting macrophage do?

A
  • collects tissue debris
  • Eliminates apoptotic cells
  • Low major histocompatibility complex (MHC) class II expression
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76
Q

What are MHC class II molecules?

A

cell membrane proteins that are specific for antigen-presenting cells such as macrophages and dendritic cells and that present antigens from ingested pathogens onto the cell surface for antigen recognition by helper T cells

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77
Q

What do primed macrophages do?

A
  • primed by interferon gamma (IFN-γ) produced by NK cells and helper T cells
  • Increased expression of MHC II
  • Increasingly phagocytotic
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78
Q

What do hyperactive macrophages do?

A
  • Stimulated with IFN-γ and lipopolysaccharide (LPS) produced by gram-negative bacteria
  • stop proliferating, become larger and very phagocytotic
  • produce cytokines: tumour necrosis factor (TNF) and interleukin-1 (IL-1)
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79
Q

Macrophage activation between the three states?

A

Resting - stimulated by IFN-γ = primed with MHC II
Resting - stimulated by IFN-γ and LPS = Hyperactive with TNF + IL-1
Primed - stimulated by LPS = Hyperactive with TNF + IL-1

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80
Q

Where do neutrophils reside? What type of white blood cell are they? How long is their life-span?

A
  • Reside in the blood
  • Macrophage
  • Short lived (5 days)
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81
Q

What is involved in the ‘double-key’ mechanism of neutrophils to infiltrate inflamed tissue from the blood?

A
  • Selectin ligand binds to selectin (present on neutrophils and expressed on inflamed vascular endothelium)
  • ICAM binds to integrin (present on endothelium and activated on stimulated neutrophils)
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82
Q

What molecules activate selectin and integrin?

A

IL-1, TNF, LPS and C5a

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83
Q

What allows neutrophil to circulate freely initially?

A

Neutrophil expresses selectin ligand (SLG) on its cell membrane and the intercellular adhesion molecule (and selectin) is expressed on the endothelial cell. These are incompatible.

84
Q

Describe the process which causes the neutrophil to slow down

A

IL-1 and TNF, stimulated by hyperactive macrophages, result in the expression of Selectin on the endothelial cell membrane to which SLG on the neutrophil binds.
The Selectin-SLG interaction is not strong enough to stop the neutrophil completely, but the cells bind and start to ‘roll’

85
Q

Describe the process in which the neutrophils stop rolling and stick to the vascular wall close to the site of infection

A
  • C5a accumulates in the inflamed tissue due to increased complement activation
  • The bacteria secretes significant amounts of lipopolysaccharide (LPS)
  • LPS and C5a activate integrin on the neutrophil
  • INT binds to ICAM which is then expressed on the endothelium = cells stop rolling and stick
86
Q

What stimulates neutrophil infiltration of the infected tissue (vascular permeability)

A

C5a and F-Met peptides stimulate this, neutrophils ‘track’ F-Met peptides.

*Human proteins = N-terminal Methionine (Met)
*Bacterial proteins = N-terminal Formyl methionine (F-Met)

87
Q

What type of white blood cell are natural killer cells? Where do they reside? Which mechanism do the use to infiltrate infected tissues?

A
  • Lymphoid
  • Reside in the blood, liver, spleen
  • ‘Roll, stop, exit’ mechanism
88
Q

What are the function of NK cells?

A
  • IFN-γ and IL-2 production
  • Apoptosis of infected cells
89
Q

How do natural killer cells trigger apoptosis of infected cells?

A
  • Fas binds Fas ligand on target cell
  • Saves healthy host cells by recognising MHC-I
  • Perforin and granzyme B are molecular messengers which induce apoptosis
90
Q

What type of molecules express MHC class I compared to MHC class II?

A
  • MHC class I expressed by all host cells
  • MHC class II (antigen presentation) expressed specifically by professional phagocytes (macrophages, dendritic cells) and antigen presenting B cells
91
Q

What do TNF and IFN reduce in the innate immune system response?

A

Reduce viral reproduction

92
Q

What is an antigen?

A

A substance that when recognised by the immune system will trigger an immune response

93
Q

What is an antibody?

A

AKA Immunoglobulin (Ig)
A specific protein made in response to an antigen, produced by B cells

94
Q

What composes the primary lymphoid tissue?

A

Bone marrow and thymus gland

95
Q

What happens in the primary lymphoid tissue?

A

Where lymphocytes develop and mature

96
Q

What composes the secondary lymphoid tissue?

A

Lymph nodes, spleen and lymphoid tissue at other sites e.g. tonsils, adenoids, Peyer’s patches

97
Q

What happens in the secondary lymphoid tissue?

A

Where lymphocytes encounter antigens/pathogens

98
Q

What are the types of B cells?

A
  • Immature
  • Transitional
  • Naïve
  • Plasma
  • Memory cells
99
Q

Where does an immature B cell develop from?

A

Stem cells in the bone marrow

100
Q

When is a B cell called an immature B cell?

A

Once it has a functional membrane B cell receptor (BCR)

101
Q

What is VDJ recombination?

A

B cells randomly rearrange their variable (V), diversity (D) and joining (J) genes to form the blueprint for the variable regions of their antibodies

102
Q

Where does diversity in VDJs come from?

A

Diversity comes from the fact that there are multiple copies of the V, D and J genes that can be joined together in different combinations.

103
Q

What is a transitional B cell a link between?

A

Link between immature B lymphocytes in the bone marrow and mature B cells in the spleen (+ maybe other secondary organs)

104
Q

What do transitional cells differentiate from?

A

Differentiate into B lymphocytes from common myeloid progenitor cells in the bone marrow, however they are not yet mature.

105
Q

Why do most transitional cells not survive to become mature B cells?

A

Many due due to high autoreactivity (self reactive BCR)

*It is thought too many transitional B cells can trigger autoimmune disorders such as lupus erythematosus and rheumatoid arthritis

106
Q

What are naïve B cells?

A

Mature B cells that have not yet been activated/ exposed to the antigen

107
Q

Where do naïve B cells reside?

A

Secondary lymphoid organs

108
Q

Once activated, what do naïve B cells become?

A

Majority become memory or plasma cells

109
Q

What are the two type of naïve B cells?

A
  • Follicular (FO) B cells
  • Marginal (MZ) B cells
110
Q

What do follicular B cells do?

A

Circulate around the body and back to the B cell areas. Go to the ‘follicular niche’ and present T-dependant antigens to helper T-cells.

111
Q

What do Marginal B cells do?

A

noncirculating in the marginal zone of the spleen, well placed to meet blood-borne antigens and become short lived plasma cells.

112
Q

What are plasma cells/effector B cells?

A

cloned daughter cells of an activated naïve B cell which do not pick up the antigen, only produce one type of antibody for one specific antigen

113
Q

At what rate do plasma cells act?

A

Very metabolically active, each cell can produce several thousand antibodies per second

114
Q

What can plasma cells become and where do they reside?

A

Can become long-lived plasma cells that reside in the bone marrow, secrete antibody and are different to memory cells

115
Q

What is the lifespan of a memory B cell compared to a plasma cell?

A

Memory B cell = longer lifespans (years)
Plasma cells = days to months

*do not yet know what causes a B cell to differentiate into either form

116
Q

How does a memory cell work?

A

Circulates around the body. Have a special affinity for one type of antigen but cannot produce antigens themselves. Second exposure to the same antigen will trigger memory B lymphocytes to divide to form plasma cells. Occurs at a more rapid rate - secondary immune response.
These plasma cells also usually have a high affinity for the antigen of interest than those from the primary response.

117
Q

What is an epitope?

A

specific part of the antigen to which the antibody binds

118
Q

What are the two routes of B cell activation?

A

T-cell independent
T-cell dependent

119
Q

What are the characteristics of the T-cell independent B-cell activation?

A
  • Contact with antigen causes B-cell activation
  • Faster but not as potent
  • Only really works for ‘conserved’ epitopes like bacterial lipopolysaccharide, polysaccharide
120
Q

What are the characteristics of T-cell dependant B cell activation?

A
  • contact with an antigen does not cause B-cell activation
  • Activation starts two processes - extrafollicular response then germinal centre response
  • CD4+ helper Th2 cells
  • Extracellular response releases loads of early weak IgM, germinal response leads to a stronger but slower response
121
Q

What are germinal centre’s?

A
  • Transient structures in secondary lymphoid organs where B cells are activated then proliferate, differentiate and perform somatic hypermutation
  • It is where T-cell dependant immune responses occur. It requires interactions between helper T-cells and mature B-cells
    Purpose of the response is to increase the affinity of antibodies produced and to generate memory cells for long lasting immune protection
122
Q

What is the purpose of the germinal centre response?

A

Purpose of the response is to increase the affinity of antibodies produced and to generate memory cells for long lasting immune protection

123
Q

What are the five steps in the germinal centre response?

A
  • T-cell dependent B-cell activation at the boundary between the T-zone/B-zone in the secondary lymphoid organ
  • Rapid proliferation and differentiation of B cells where they go through somatic hypermutation. These B cells are called centroblasts
  • Centroblasts move from the dark zone to the light zone and start to express these mutated antibodies. When they are presenting the mutated receptor on their surface they are called centrocytes. Those with higher affinity bind to the antigen and helper T cells better survive, those that don’t go through apoptosis.
  • These centrocytes go back into the dark zone, become centroblasts and will go through more rounds of somatic hypermutation
  • Cytokine release by the T-cell also triggers switching of immunoglobulins (IgD/IgM to IgA/IgG/IgE). The class they switch to is normally dictated by the particular cytokines in the local environment.
124
Q

What types of mutations are somatic hypermutations usually?

A

Mutations are usually substitutions rather than insertions/deletions

*Lots of mutations, easy source for malignancy to start

125
Q

Where do somatic hypermutations occur?

A

Occur at hotspots involved in antigen recognition

126
Q

Which enzyme causes a somatic hypermutation?

A

Activation-induced cytidine changes a cytosine to a uracil. This is repaired but not always properly.

127
Q

Describe the structure of an antibody

A

4 chains - 2 heavy and 2 light. In each heavy chain there are 4 domains - 3 constant, 1 variable and in each light chain there are 2 domains - 1 variable and 1 constant

128
Q

What is the Fab (antigen-binding fragment)

A

The top half (1 variable region and 1 constant of each light and heavy) is the Fab. At the top of the Fab is the Fv region (binding region). The variability is created by randomly assigning V.D.J. segments.

129
Q

What are the 7 antibody types?

A
  • IgG
  • IgA
  • IgM
  • IgE
  • IgD
  • Monoclonal
  • Polyclonal
130
Q

What do IgM antibodies do?

A
  • Monomer form is the BCR (beta cell receptor) on mature B cells
  • Involved in primary response
  • Causes many types of antigens to clump together
  • Can bind complement, activating classical pathway
131
Q

Where do IgM antibodies circulate and what shape are they?

A
  • Largest antibody, usually a pentamer
  • Usually in the blood, too big to get into tissue
132
Q

What are the characteristics of IgG antibodies?

A
  • Most common immunoglobulins in the blood
  • Predominantly involved in the secondary immune response
  • Can enter tissue space
  • Only immunoglobulin that can cross the placenta
  • Has 4 subclasses
133
Q

What are the characteristics of IgG antibodies?

A
  • Most common immunoglobulins in the blood
  • Predominantly involved in the secondary immune response
  • Can enter tissue space
  • Only immunoglobulin that can cross the placenta
  • Has 4 subclasses
134
Q

What do IgG antibodies do?

A
  • Binds to a variety of pathogens
  • Causes agglutination and opsonisation
  • Can neutralise toxins (no longer infectious or pathogenic)
  • Activates complement system
  • Marks cells for cell lysis by NK cells
135
Q

What do IgD antibodies do?

A
  • Functions as a receptor to activate B cells
  • Usually co-expressed with IgM
136
Q

What do IgE antibodies do?

A
  • Involved in parasitic worm defence
  • Binds to mast cells, causing histamine release
  • Involved in allergic reactions and can cause anaphylaxis
137
Q

Where are IgA antibodies found?

A

Secretory fluids such as sweat, tears, saliva and in mucosal surfaces. Monomer in blood.

*High concentration in breast milk giving immunity to new-borns

138
Q

What shape are IgA antibodies and why is this important?

A

Dimer structure allowing it to survive in harsh conditions

139
Q

Which immunoglobulin is produced most?

A

IgA

140
Q

What are the functions of IgA immunoglobulins?

A
  • Main function here is to stop pathogens binding to cell surface receptors, rather than marking the pathogen for death
  • Similar function to IgG
141
Q

What are polyclonal antibodies?

A

Represents collection of antibodies from different B cells that recognize multiple epitopes on the same antigen.
Each of these individual antibodies recognizes a unique epitope that is located on that antigen. Increased chance of cross-reactivity with similar antigens.

142
Q

What are monoclonal antibodies?

A

Represents antibody from a single antibody producing B cell and therefore only binds with one unique epitope.

143
Q

What is the primary response?

A

The first time the body encounters an antigen. Naïve B-cells activated and become plasma and memory cells (4-7 days).
Antibody titre is low, main type is IgM and lasts 7-10 days. Stay present for weeks/months.
Antibodies produced are of low affinity, occurs in lymph nodes and spleen

144
Q

What is the secondary response?

A

Any subsequent exposure and is T-cell dependent.
There are memory cells so faster response (1-4 days) and larger (100-1000 times)
IgG is main type but others produced.
Stay for longer than the primary response
Antibodies are of higher affinity and in the bone marrow (where memory cells are)

145
Q

What are the three types of T-cells?

A
  • T helper cells (CD4+)
  • T killer cells (CD8+)
  • T regulatory cells (CD4+, CD25+, FOXP3+)
146
Q

What do T-helper (CD4+) cells do?

A
  • help one another
  • activate B cells
  • activate phagocytes
  • T helper cells produce Th1 and Th2 cytokines that augment cell mediated and humoral immunity respectively
147
Q

What do T killer (CD8+) cells do?

A
  • cytotoxic T lymphocytes (Tc) (CDG +ve)
  • Effective at attacking viruses
148
Q

What do T-regulatory (CD4+, CD25+, FOXP3+) cells do?

A
  • FOXP3+ is not fully understood
  • regulate or suppress other cells in the immune system
  • protect against autoimmune system
149
Q

What do T-cells need to be activated?

A

need antigens presented by APCs coupled with an MHC molecule, otherwise can’t recognise or respond to them

150
Q

What do T-cells mainly do once they are presented with the antigen and activated?

A
  • Boost the immune response e.g. release IFNg activating macrophages (CD4+ and CD8+)
  • Kill directly (CD8+)
151
Q

What happens after T-cells have an antigen presented to them?

A
  • T cell receptor (TCR) is associated with CD3 molecule (CD3/TCR complex)
  • TCR from T cell binds with MHC on the APC
  • CD8+ cells bind to MHC1 on the surface of other cells.
    CD4+ binds to MHC2 on the surface of other cells. (81 or 42)
  • MHC1 “window into a cell” - intracellular antigens are presented
  • MHC2 presents extracellular antigens.
152
Q

What is ‘cross-presentation’ by dendritic cells?

A

Presenting intracellular antigens on MHC2 and vice versa

153
Q

How do dendritic cells form epitopes?

A

Inflammation causes dendritic cells to consume the antigen, process it through lysosomes called the immunoproteasome then present these digested products via MHC complexes, these digested antigens are now epitopes.

154
Q

What is involved in signal 1 of T-cell activation?

A

The T-cell receptor recognises the antigen presented in the MHC

155
Q

What is involved in signal 2 of T-cell activation?

A

CD28 on T cell binding to CD80/CD86 on the antigen presenting cell. This process is modulated by CTLA-4, which is present on the T-cell.

156
Q

Why is second signal for T-cell activation needed?

A

To prevent T cells being activated by the body’s own (host) antigens, would lead to an autoimmune response.
If Th cell recognised a host peptide presented with an MHC molecule on the surface of a cell, that could lead to such a response. Only when the presentation is made by an APC, with the necessary CD80 molecule as well, will the Th cell be activated.
As APCs are only presenting foreign antigens that they have ingested, this prevents activation by host antigens. Without this the T cell will become anergic, meaning that it does not respond to the antigen.

157
Q

What is involved in signal 3 of T-cell activation?

A

additional receptors like PD1/PD-L1 or cytokines released from other cells in the local area. In the case of helper T cells, this pushes them towards a Th1 or Th2 response and further activates the cytotoxic T-cells

158
Q

What is central tolerance?

A

Occurs via negative immune selection in the primary lymphoid organs.
Occurs for both T-cells and B-cells

159
Q

What happens in positive selection of central tolerance?

A

Positive selection in the thymic cortex (thymus) involves a check to see if T-cell can bind to MHC1 or MHC2. If they can’t they die of apoptosis. Depending on which it binds to better, it’ll become CD4+ or CD8+ T cell.

160
Q

What happens in negative selection of central tolerance?

A

T-cells are tested for affinity to bind to self antigen. If they bind to a self antigen they undergo apoptosis. Thymic epithelial cells present the self antigens. Occurs in the cortico-medullary and thymic areas.

161
Q

What is tolerance?

A

Process by which the immune system prevents recognition of self antigens and immune response to it

162
Q

Describe central tolerance in the bone marrow

A

Occurs with B cells
- Clonal deletion when cells encountering self are recognised
- Further B cell receptor gene editing
(Ig gene rearrangement)

163
Q

Describe central tolerance in the thymus

A

Occurs with T-cells
- Positive selection: only cells recognising MHC survive
- Negative selection: cells recognising self antigen (clonal deletion)

164
Q

Why is peripheral tolerance needed?

A

Not all T-cells that are self reactive are picked up by central tolerance. Can cause autoimmunity

165
Q

What is T-cell anergy?

A

Tolerance mechanism where the lymphocyte is intrinsically functioning inactivated following an antigen encounter, but remains alive for extended period of time in a hyporesponsive state.

166
Q

How does anergy play out in signal 2 and 3 of T-cell activation?

A
  • Upon recognising self antigen there are no co-stimulatory molecules (signal 2)
  • If there is no local inflammation there will be no cytokines (signal 3). This process is reversible.
167
Q

What is an example of peripheral tolerance by anatomical barriers and immune privileged areas?

A

Inside the eyes (injury to one eye can cause immune destruction to the other eye)

168
Q

What antigen is present on the HIV virus?

A

gp120

169
Q

What is the receptor for the HIV antigen?

A

CD4 forms the receptor for this antigen (virus is attached to CD4 cells). Can also bind to CCR5 or CXCR4

170
Q

How are viral genes created

A

Virus injects its RNA and reverse transcriptase into the cytoplasm (transforms RNA to DNA) and forces the cell to make viral genes and forget about its own functions.

171
Q

Transmission response against HIV infection?

A

Initially met by dendritic cells that process virus. Take it to a lymph node where it comes into contact with CD4+ cells. This causes an immune response causing fever.

172
Q

Dissemination response against HIV infection?

A

Germinal centres response causes lymphadenopathy. HIV infected CD4+ cells migrate around the body and viral load increase. HIV starts to infect macrophages that express CD4 and CCr5. DCs that are not CD4+ can capture and present antigen to these cells

173
Q

Control response against HIV infection?

A

Cross presentation by DCs causes a robust HIV-specific CD8+ Tcell response causes drop in viral loads by killing infected CD4+ cells. By killing infected CD4+ cells, the overall population increases but never back to baseline.

174
Q

Seroconversion response against HIV infection?

A

Antibodies to HIV occurs 4-6 weeks after transmission. This needs HIV-specific helper T cell and presentation by DCs in the lymph nodes

Neutralising antibodies occur 3-6 months later

During chronic infection, immune exhaustion results in opportunistic infection and AIDs

175
Q

What is a hypersensitivity reaction?

A

Over reaction of immune response causing tissue damage

176
Q

What are the sub-classifications of hypersensitivity reactions and what are the descriptions?

A
  • Autoimmunity = Hypersensitivity reactions against self-antigens
  • Allergy = Hypersensitivity reactions against certain exogenous antigens
177
Q

What is the mechanism for IgE mediated hypersensitivity Type 1?

A

Exposure to allergen = allergen binds to IgE on mast cells = IgE cross linking  triggers ‘degranulation’
= release of molecules

178
Q

What molecules are released in the IgE mediated hypersensitivity Type 1 mechanism?

A
  • histamine = vasodilation/SM contraction
  • Eosinophil/neutrophil chemotactic agent = increased inflammatory cells
  • Proteases = tissue damage
  • other mediators
179
Q

What are examples of hypersensitivity?

A
  • Eczema
  • Asthma
  • Hay fever
  • Anaphylaxis
180
Q

Which antibody mediates a Type 2 hypersensitivity reaction?

A

cytotoxic/ antibody IgM or IgG

181
Q

What is the mechanism for Type 2 hypersensitivity reactions?

A

Bind to target antigen on cell surface which triggers one of three mechanisms:
- Cytotoxic T-cells bind to Ab = release of perforin/granzymes = apoptosis of cell

  • Activate complement pathway
    1) Complement binds to antibodies (opsonisation)= phagocyte binds = cells is phagocytosed
    2) Complement forms membrane attack complex = osmotic swelling of cell = Cell lysis
    3) Complement acts a chemotactic agent = increased inflammatory cells in tissues = tissue damage
  • Antigen is a cell surface receptor = Ab activates/ blocks normal receptor = altered function of cell.
182
Q

What are examples of Type 2 hypersensitivity?

A
  • Graves Disease
  • Blood transfusion reactions
183
Q

What mediates type 3 hypersensitivity reaction?

A

Immune complex mediated

184
Q

What is the mechanism for the type 3 hypersensitivity reaction?

A

Increased antibody production in response to antigen = antibodies enter blood and bind to soluble antigens = immune complexes form = immune complexes get lodged in basement membrane of blood vessels = activates the complement cascade

185
Q

What are examples of type 3 hypersensitivity reactions?

A
  • Lupus
  • Rheumatoid arthritis
186
Q

How is type 4 hypersensitivity mediated?

A

cell mediated/delayed

187
Q

How does sensitisation during type 4 hypersensitivity occur?

A

First exposure to antigen = engulfed by antigen presenting cells = antigen ‘presented’ to naïve CD4 positive T cells = naïve cell matures into TH1 cell

188
Q

What happens once sensitised in the type 4 hypersensitivity reaction?

A

Repeat exposure to antigen = antigen binds to sensitised TH1 cells = cytokines released =
- Activation of macrophages = release proinflammatory cytokines/ enzymes
- Activation cytotoxic T cells = direct cellular damage

189
Q

What are examples of type 4 hypersensitivity?

A
  • Coeliac disease
  • Type 1 diabetes
190
Q

What is the cause of autoimmune disease?

A

Arise due to type II/II/IV hypersensitivity reactions against self antigens

191
Q

When and where does central tolerance occur?

A

In bone marrow/ thymus when self lymphocyte is maturing

192
Q

When and where does peripheral tolerance occur?

A

If self lymphocyte escapes into circulation/other tissues

193
Q

Which demographic are autoimmune diseases most common in?

A

More common in younger women

194
Q

How are autoimmune diseases treated?

A

Often treated with immunosuppression

195
Q

Characteristics of autoimmune diseases (causes)

A
  • mixed multifactorial environmental/genetic aetiology
  • Overlap between other autoimmune conditions
196
Q

3 examples of autoimmune diseases and what do they do?

A
  • lupus = antibodies against substances from nucleus eg anti dsDNA
  • type 1 diabetes mellitus = antibodies against islet cells in pancreas
  • graves disease = thyroid stimulating antibodies
197
Q

What are examples of allergic reactions (and their allergens) with increasing severity?

A

1) Hay fever (allergic rhinitis) = pollen
2) Eczema (atopic dermatitis) = soaps/detergents
3) Allergic asthma = dust/animal fur
4) Hives (urticaria)
5) Angioedema
6) Anaphylaxis

4, 5 and 6 have allergens that are food/drugs/insect bites

198
Q

What is the atopic triad?

A

When asthma, eczema, hay fever occur in the same patient

199
Q

What is the atopic march?

A

Describes natural history of these conditions

200
Q

What are the symptoms of anaphylaxis

A

*Anaphylaxis is a severe and life threatening allergic reaction
- Low blood pressure (shock)
- Shortness of breath/wheezing
- Loss of consciousness
- +/- angioedema, hives

201
Q

What is immunodeficiency?

A

When a person has an absent or defective immune response. Can be classified as either primary or secondary.

202
Q

What are examples of primary (genetic) immunodeficiency?

A
  • Di George Syndrome = small or absent thymus
  • SCID (severe combine immune deficiency) = lots of problems, inability for T cells to survive
    -CVID (common variable immune deficiency) = low antibodies
203
Q

What are examples of secondary (acquired) immunodeficiency?

A
  • malnutrition
  • drugs (chemotherapy for cancer, anti-rejection drugs, drugs to treat autoimmune conditions, steroids)
  • HIV/AIDS
204
Q

What cells do HIV/AIDS infect and what occurs?

A
  • Infects CD4+ T helper cells
  • Takes over function of T cell to enable viral replication
  • T cell function (and CD4 count) falls with time
  • Increased risk of opportunistic infections
205
Q

What is the role of a vaccine?

A
  • to ‘teach’ the immune system to create specific memory cells without needing to suffer disease
  • means if exposed to pathogen = no/milder disease develops
  • variable length of protection e.g. flu vaccine
206
Q

What are the vaccine types and examples?

A

1) The whole microbe
- Inactivated/killed e.g. Hep A
- Live-attenuated e.g. MMR
- Viral vector e.g. AstraZeneca COVID

2) Part of the microbe
- Subunit/acellular e.g. Pertussis

3) genetic material of the microbe
- mRNA e.g. Pfizer COVID

207
Q

What might stope a patient getting a vaccine?

A
  • Patient preference
  • Live viruses in immunocompromised patients
  • Allergy to ingredient in vaccine

Med Year 1 - IMS (9 decks)

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