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Block 2 > Introduction To The Immune System > Flashcards

Introduction To The Immune System Flashcards

1
Q

List the 4 roles of the immune system.

A
  1. Immunity to infection
  2. Inflammatory processes
  3. Removal of senescent cells
  4. Defence against neoplasia
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2
Q

Why is immunology medically relevant?

A

Immune disorders e.g. immunodeficiency (primary/secondary) + autoimmunity

Immunology tests e.g. serology + cross-matching/tissue-typing

Immunotherapies e.g. hypersensitivity (desensitisation) + cancer (IL-2 for melanoma + renal cancer)

Immunoprophylaxis e.g. vaccine against infections + cancer (e.g. prostate)

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3
Q

Define antigen.

A

Immune functions are responses to antigens which are defined as:

Any substance capable of inducing a specific immune response

E.g. molecules on microbes, neoplastic cells + foreign tissues

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4
Q

What are self-antigens?

A

Antigens that are usually tolerated by the immune system

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5
Q

Why are antigens recognised by the immune system?

A

Because some are very obviously different from host molecules and are called Pathogen-Associated Molecular Patterns (PAMPs) e.g. bacterial peptidoglycan, lipopolysaccharide (LPS) + flagellin

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6
Q

Why do some antigens avoid the immune response?

A

They may mimic normal tissue, be subtly different to self-antigens or be variable in their make-up

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7
Q

What are the 2 different approaches to the immune system?

A
  1. Structural: classified via spread throughout the body but this is not useful as immune response composed of cells (often in groups) + chemicals (humoral factors)
  2. Functional: classified into “innate” + “adaptive” components
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8
Q

Antigens with PAMPs are mostly target by __ ___ whilst other antigens are mostly targeted by __ ___.

A

Innate mechanisms

Adaptive mechanisms

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9
Q

What are the 6 main features of the innate immune response?

A
  1. Primary line of defence
  2. Immediate response
  3. Recognises certain threats
  4. No antigen presentation
  5. No clonal selection
  6. No immunological memory
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10
Q

What are the 6 main features of the adaptive immune response?

A
  1. Secondary line of defence
  2. Delayed response
  3. Recognises all threats
  4. Antigen presentation
  5. Clonal selection
  6. Immunological memory
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11
Q

What is clonal selection?

A

Where the adaptive immune response will select the best clones of cells to deal with a specific antigen and cause them to replicate

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12
Q

What are the components of the innate immune system?

A 
Epithelial barriers
Phagocytes
Dendritic cells
Complement
Acute Phase Proteins (APP)
NK cells
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13
Q

What are the components of the adaptive immune system?

A

B lymphocytes
Antibodies
T lymphocytes
Effector T cells

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14
Q

What are the 6 components of the immune system?

A
  1. Cells (mostly leukocytes)
  2. Neutrophils: polymorphonuclear (PMN) phagocytes/granulocytes
  3. Lymphocytes: T (cytotoxic, memory, helper + suppressor) + B (plasma + memory cells)
  4. Monocytes + macrophages: mononuclear phagocytes (APCs)
  5. Eosinophils
  6. Basophils + mast cells
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15
Q

What responses are eosinophils involved in?

A

To parasites infections + allergic responses

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16
Q

What responses are basophils + mast cells involved in?

A

Inflammatory + hypersensitivity responses

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17
Q

What is the difference between monocytes + macrophages?

A

They are the same but macrophages are the blood version of the cell whilst monocytes have gone from the blood into tissues

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18
Q

What are the 9 tissue/organ components of the immune system?

A
  1. MALT (adenoids + tonsils)
  2. Thymus (T lympho maturation)
  3. BALT (macrophages)
  4. Lymph nodes (small collection of lymphoid tissue)
  5. Kupfer cells (macrophages) of liver
  6. Spleen (large collection of lymphoid tissue)
  7. GALT (Peyer’s patch in SI, appendix + LI)
  8. Bone marrow (haematopoiesis + B lympho maturation)
  9. SALT (dendritic cells - macrophages)
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19
Q

What are the 4 classes of humoral factors in the immune system?

A
  1. APPs e.g. α, β, γ-globulins
  2. Complement e.g. C1-9 (5b-9 = MAC)
  3. Antibodies e.g. IgM, IgG, IgA, IgE, IgD
  4. Cytokines e.g. ILs, IFNs
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20
Q

How is the complement cascade triggered?

A

PAMPs on pathogens can trigger it directly (innate)
OR
Abs can link complement to the pathogen (adaptive)

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21
Q

What are the functions of cytokines?

A

Control of immune system e.g. up-regulation, chemotaxis + viral resistance

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22
Q

What are the main structural features of antibodies? What is the importance of this?

A

Heavy + light chain
Constant region
Variable region at top because each Ab will bind a different Ag

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23
Q

What antibody is the first one produced in an immune response?

A

IgM

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24
Q

What antibody tends to be released into the gut?

A

IgA

25
Q

What are the 4 most common mucosal surfaces for infectious agents to get in by?

A
  1. Nasopharynx
  2. Respiratory tract
  3. Alimentary tract
  4. Genito-urinary tract
26
Q

What are the 2 different types of barriers of barrier immunity? Give examples.

A
  1. Physical barriers e.g. skin, mucus, respiratory cilia + commensal organisms
  2. Biochemical barriers e.g. sebaceous secretions in skin, lysozyme in tears, spermine in sperm + gastric acidity
27
Q

Define phagocytosis. What are the 2 main cell types involved?

A

Recognition + engulfing of microbes which are then killed by the release of toxic chemicals (oxidative burst) into the enclosed vacuole that they are within

  1. PMN leukocytes = neutrophils
  2. MPS = monocytes + macrophages
28
Q

What occurs in the innate cell-mediated immune response?

A

Neutrophils (have rapid action) + monocytes/macrophages engulf microbes (especially if “opsonised by complement or Ab)

NK cells detect lack of MHC class I on cells (infected/malignant) through lack of stimulation of inhibitor receptors, activating them -> pore-forming molecules inserted into target cell + cytotoxic chemicals pumped in

29
Q

What clinical issues can arise if there is a problem with the phagocytosis aspect of innate cell-mediated immunity?

A

Neutropenia can occur during chemotherapy for malignancies -> “neutropenic sepsis” = life-threatening emergency

Genetic inability to produce toxic chemicals within phagocytes = immunodeficiencies e.g. CGD

30
Q

What are the steps of phagocytosis?

A
  1. Chemotaxis + adherence of microbe to phagocyte
  2. Ingestion of microbe by phagocyte
  3. Formation of a phagosome
  4. Fusion of phagosome with a lysosome -> phagolysosome
  5. Digestion of ingested microbe by enzymes
  6. Formation of residual body containing indigestible material
  7. Discharge of waste materials
31
Q

What are Natural Killer (NK) cells?

A

Lymphocytes that perform both direct + antibody-dependent cell cytotoxicity (process remains innate)

32
Q

What is the clinical relevance of the NK cell aspect of innate cell-mediated immunity?

A

NK cells deficient in genetic diseases affecting T lymphocytes e.g. X-linked lymphoproliferative syn. -> fatal EBV infections

Laboratory activated NK cells being used in cancer trials

33
Q

What does the Acute Phase Proteins (APPs) do in the innate humoral immune response?

A

Cells of innate IS have PRRs to recognise PAMPs -> 2-100x increase in blood APPs (e.g. CRP, procalcitonin, ALP + ferritin) = immediate/non-specific cytotoxicity

E.G. CRP binds to surface molecules of bacteria + fungi -> inhibitory effects + promotes complement binding (so CRP is useful marker of bacterial infection)

34
Q

What does the complement aspect of innate humoral immunity do?

A

Complement = 20 different β-globulins found in blood mostly produced by liver + work in a cascade

Alternative pathway (Ab independent cell lysis) + classical pathway (Ab dependent cell lysis)

35
Q

What is the step-by-step mechanism of the alternative complement pathway?

A
  1. C3 cleaved in presence of microbial components
  2. C3a released -> chemotaxis + local anaphylaxis
  3. C3b attaches to microbe -> opsonisation + C5 cleavage
  4. C5a released -> chemotaxis + local anaphylaxis
  5. C5b attaches to microbes + activates C6, 7, 8 + 9
  6. C5b, 6, 7, 8 + 9 = MAC -> cell lysis

Other components interact with coagulation + fibrinolysis cascades

C1 inhibitor + other factors needed to restrain pathway

36
Q

What is the difference in the classical pathway of complement in comparison to the alternative pathway?

A

It begins with Ag binding Ab (adaptive) which binds a C1 complex. C2a + C4b fragments are released and then C3 convertase cleaves C3. The pathway then continues as the alternative pathway ending in cell lysis.

37
Q

How is C3 cleavage inhibited normally? How do these regulatory mechanisms stand by when complement needs to occur?

A

C3 cleavage is inhibited by factor H + I

These factors are blocked by microbial components e.g. LPS allowing complement cascade to move forward

38
Q

What is the third way in which complement can be activated?

A

Mannose-binding lectin in the lectin pathway

39
Q

What are the main humoral factors of complement and their functions?

A

C3a + C5a: inflammation

C3b: opsonization + phagocytosis of microbes

40
Q

What are Major Histocompatibility Complex (MHC) molecules? What are the 2 different types?

A

Same as HLA system; MHC present Ags from inside cell for inspection

Class I (on all cells except RBCs): present host, viral or neoplastic Ags to Tc lymphos (cytotoxic action)

Class II (on APCs): present ingested microbial Ag to Th lymphos (interact with B lymphos to produce Ab)

41
Q

What is the clinical relevance of MHC molecules?

A

MHC/HLA genetic variations associated with immune-mediate diseases e.g. ankylosing spondylitis (HLA B27)

MHC/HLA matching important in organ transplantation

42
Q

What is the name of the process whereby T cell receptors bind MHC molecules on cells?

A

MHC restriction

43
Q

What are the end points of antigen presentation via MHC class I and II?

A

Class I: killing of Ag-expressing infected cell by Tc’s

Class II: Cytokines cause macrophage activation + destruction of phagocytosed microbes OR B cell Ab secretion + Ab binds microbe

44
Q

What is involved in the adaptive cell-mediated immune response?

A

Tc cells

Cells present Ag on MHC class I to Tc cells -> those that recognise foreign Ag replicate + differentiate

Activated Tc cells attack host cells that present Ag via cytotoxicity + memory Tc cells maintain immunological memory of Ag

45
Q

What cells influence Tc cell activity?

A

T-helper cells

T-suppressor cells

46
Q

What is the benefit of genetic recombination of Tc lymphocytes + B cells?

A

Each Tc cell will recognise a single Ag + when it recognises that Ag, there is clonal selection + expansion ensuring a specific response + memory

Each B lympho recognises a single Ag so when it is present, there is clonal selection + expansion ensuring a specific response + memory

47
Q

What is the clinical relevance of the adaptive cell-mediated + humoral immune response?

A

Th (CD4) cells are targets of HIV + die when infected so adaptive cell-mediated + humoral immunity is compromised by HIV infection

48
Q

What is involved in the adaptive humoral immune response step-by-step?

A
  1. Microbes phagocytosed by APCs (from MPS)
  2. APCs present Ag via MHC class II to Th cells
  3. Same Ag stimulates B lymphos (with Th support) + those that recognise Ag replicate + differentiate
  4. B plasma cells produce Ab that attack only that Ag + B memory cells maintain immunological memory of Ag
49
Q

How can the immune system be controlled?

A

IS must be turned on + off to varying degrees so there is:

  • Stimulating factors (e.g. presence of Ag, Th cells + cytokines)
  • Inhibiting factors (e.g. removal of Ag, Ts cells + cytokine breakdown)

Also clonal selection allows fine tuning of immune response (increased affinity) + memory cells improve response to same Ag in future

Many diseases exist due to problems controlling IS

50
Q

Control system overlaps with those for ____ + ____.

A

Inflammation

Coagulation

51
Q

In terms of immune system control, what does tolerance of own antigens seem to rely on?

A

Pre-natal exposure + continuous large scale re-exposure to own Ags

52
Q

How does immunological memory work in the adaptive immune response?

A

Primary response: occurs at 5-10 days + carried out by IgM -> Abs have lower affinity + are more variable

Secondary response: occurs at 1-3 days (quicker) + carried out by IgG (sometimes IgA or IgE too) -> larger response 2nd time round + higher average affinity (affinity maturation)

53
Q

What are the 2 mechanisms of immunological tolerance of T cells in the thymus?

A
  1. Negative selection/deletion: some autoimmune T cells destroyed before birth in utero as at this point, everything is a self Ag (no infection)
  2. Development of regulatory T cells: autoimmune cells regulated as IS knows they exit before birth so keep close tabs on them
54
Q

What are interleukins and how do they control the immune system?

A

12 different ILs produced by MPS + Th cells that stimulate various components of IS -> proliferation, differentiation, activation + chemotaxis

Involved in every step of adaptive immunity having a short-lived autocrine + paracrine effects (local effects)

55
Q

What is the clinical relevance of interleukins (ILs)?

A

Recombinant IL-2 used in some cancer treatments

56
Q

What is Tumour Necrosis Factor (TNF)? How does it control the immune system?

A

Small protein produced by MPS cells having multiple effects on various cells -> fever, inflammation, enhanced immunity, septic shock, anorexia + cachexia

So anti-TNF drugs useful in treatment of autoimmune diseases (e.g. RA) but can cause reactivation of latent infections (e.g. TB)

57
Q

What are interferons (IFNs)? How are they used to control the immune system?

A

3 different proteins (α, β + γ) produced by virus-infected cells + Th cells -> activate NK + Tc cells = cell cytotoxicity + viral resistance in other host cells

Also activate macrophages + upregulate antigen presentation interacting with adaptive IS

58
Q

What is the clinical relevance of IFNs?

A

Recombinant IFN preparations are used as medicines e.g:

  • αIFN - chronic viral hepatitis
  • βIFN - aggressive forms of MS
  • γIFN - CGD + osteoporosis

Adverse effects include “flu-like” symptoms

Block 2 (45 decks)

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