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FUNMED > Immunology > Flashcards

Immunology Flashcards

1
Q

What is SCID?

A

Severe combined immune deficiency - individual doesn’t have any lymphocytes

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2
Q

What is primary lymphoid tissue?

A

Bone marrow and thymus

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3
Q

What is secondary lymphoid tissue?

A

Tonsils, lymph nodes, lymph vessels, liver, spleen, Peyer’s patch (small intestine) and appendix

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4
Q

Define ‘antigen’

A

Anything which elicits an adaptive immune response

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5
Q

Define ‘self-antigen’

A

When immune system goes awry and starts recognising own cells as foreign

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6
Q

Define ‘inflammation’

A

When white cells leave the blood and move into tissues to get rid of pathogens and kill normal tissue in the process as well

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7
Q

How do lymphocytes respond to foreign molecules?

A

Antigen-specific receptors (BCR/TCR)

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8
Q

How do phagocytes respond to foreign molecules?

A

Have pattern recognition receptors and Fc receptors which react to PAMP structures on foreign molecules

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9
Q

What are the first cells to respond to an infection?

A

Neutrophils –> bacteria phagocytosed and killed

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10
Q

Describe how the immune system responds to a nail through the skin

A

Neutrophils (phagocytose and kill bacteria) –> skin macrophage releases TNF-alpha and IL-1beta to increase stickiness of endothelial by increasing number of adhesion molecules –> lymphocyte recruitment

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11
Q

Name some ‘pathogen-associated molecular patterns’ (PAMPs) that can be recognised by phagocytes

A

flagella, double-stranded viral RNA, lipoproteins and CpG DNA

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12
Q

What happens if a cell recognises any PAMPs?

A

Starts to produce pro-inflammatory cytokines

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13
Q

Where do T cells mature?

A

Thymus

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14
Q

Describe neutrophils

A

Full of dangerous molecules and die in the tissues e.g. free radicals, collagenase and cytokines

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15
Q

What controls T cell expansion?

A

IL-2

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16
Q

What happens when T cells are activated?

A

Clonal expansion (IL-2 needed_ then memory T-cells are produced too

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17
Q

Define ‘epitope’

A

Portion of an antigen that is recognised and bound by a receptor on an immune cell (antigens can contain many epitopes)

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18
Q

What is the innate immune system?

A

NK cells, monocytes, granulocytes and dendritic cells

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19
Q

What is the adaptive immune system?

A

T and B cells

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20
Q

What does TLR4 do?

A

Present on macrophages and dendritic cells, toll-like receptor 4 binds LPS (a form of PAMP)

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21
Q

What are B cell receptors made of?

A

They are immunoglobulins/antibodies

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22
Q

What are the 4 different isotopes of antibody?

A

IgA, IgE, IgM, IgG

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23
Q

What is meant by ‘class switching’?

A

Given B cell will begin by making IgM and this is the default that must be changed

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24
Q

How are antigens presented to T cells?

A

By dendritic cells on MHC/HLA complex

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25
Q

What codes for the composition of the TCR?

A

α-chain locus is on chromosome 14, β-chain locus is on chromosome 7

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26
Q

How is receptor diversity generated in antibodies?

A

Somatic DNA recombination, mixing and matching within heavy and light chain loci genes, and random mixing and matching of the variable, diversity and joining segments

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27
Q

What codes for the composition of MHC/HLA?

A

α and β chains in MHC found on chromosome 6

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28
Q

Why is MHC binding termed ‘promiscuous’?

A

Binds to a range of peptides that can be accommodated in the groove, not just a single peptide

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29
Q

Name two properties of MHC

A

Polygenic, polymorphic

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30
Q

Define ‘polygenic’

A

Phenotypes influenced by more than one gene

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31
Q

Define ‘polymorphic’

A

Occurring in several different forms

32
Q

Describe MHC Class I

A

All cells present molecule, and presents antigens to CD8 T cells.

33
Q

What are the types of MHC Class I?

A

HLA-A/B/C

34
Q

Describe MHC Class II

A

APCs only present this molecule, and antigens are presented to CD4 T cells

35
Q

What are the types of MHC Class II?

A

HLA-DQ/DR/DP

36
Q

Which HLA/MHC molecules are present in coeliac disease?

A

HAL-DQ2/DQ8

37
Q

Define ‘central tolerance’

A

As T and B cells develop (thymus and bone marrow respectively), their receptors are tested for reactivity to self-antigens, if too strong –> destroyed

38
Q

Define ‘peripheral tolerance’

A

Self-reactive lymphocytes which escape destruction can be controlled by T regulatory cells

39
Q

Which molecules target epithelial surface infections?

A

IgA and antimicrobial peptides

40
Q

What is a ‘humoral immune response’?

A

Transformation of B cells –> plasma cells to produce and secrete specific antibodies to pathogen

41
Q

What do antibodies do?

A

Neutralise toxins, agglutinate, opsonise (make cell more susceptible to be phagocytosed), activation of complement, antibody-dependent cell killing (NK cells)

42
Q

Define ‘complement’

A

Group of proteins present in blood plasma and tissue fluid which combine with antigen-antibody complexes to bring about lysis of foreign cells

43
Q

What is the response to cytoplasmic infections?

A

CD8 and NK T cells

44
Q

What is the response to vesicular infections?

A

T cell-dependent macrophage activation

45
Q

What is ‘cell-mediated immune response’?

A

Response produced when sensitised T cells directly attack foreign antigens and secrete lymphokines

46
Q

Why can CD8 T cells induce apoptosis?

A

TCRalphabeta and a CD8 co-receptor

47
Q

Describe the cell-mediated immune response

A

Dendritic cells engulf and present antigens –> enter lymph nodes via afferent route –> CD8 T cells leave lymph node via efferent route –> direct cytotoxic activity on invading pathogens –> induce apoptosis in infected cells due to TCRab and CD8 co-receptor

48
Q

Describe what happens in apoptosis

A

Nuclear blebbing, alteration in cell morphology, shedding of small membrane vesicles, DNA fragmentation (nuclease enzymes), apoptotic bodies are removed by phagocytic cells

49
Q

What two enzymes allow CD8 T cells to induce apoptosis?

A

Perforin and Granzymes

50
Q

Describe how CD8 T cells induce apoptosis

A

1) Non-specific adhesion between target cell and CD8 cell
2) TCR-MHC interaction –> specific binding
3) Reorganisation of microtubule-organising centre and Golgi of CD8 cell
4) Lytic granules are released (granzyme and perforin)
5) Cell death of target cell (apoptosis)

51
Q

What does perforin do?

A

Modifies target cell by forming pores in cell membrane

52
Q

What do granzymes do?

A

Proteases which chop up proteins in target cell

53
Q

What are natural killer cells?

A

Innate immune system, don’t have antigen-specific receptors and kill by same means as CD8 T cells (granzyme and perforin)

54
Q

How are NK cells activated?

A

By cytokines to cause the release of interferon gamma which increases NK killing efficiency

55
Q

How do NK cells identify cells to kill?

A

Missing-self hypothesis - has activating and inhibiting receptors: if cell has MHC Class I receptor then it will recognise as self (inhibitor, even in spite of any activation), if cell doesn’t have MHC Class I receptor –> apoptosis via lytic granule release

56
Q

What do Th1 cells do?

A

Drive cell-mediated immunity to activate macrophages

57
Q

What do Th2 cells do?

A

Drive humoral immunity to help B cells make antibodies

58
Q

What do Th17 cells do?

A

Drive responses to extracellular bacteria

59
Q

What do T-reg cells do?

A

Retrain immune responses

60
Q

What do Th1 cells produce?

A

IFN-gamma (activates macrophages)

61
Q

What do Th2 cells produce?

A

IL-2,4,5,13

62
Q

When do Th0 cells differentiate into Th1 cells?

A

presence of IL-12/13 (produced by dendritic cells)

63
Q

When do Th0 cells differentiate into Th2 cells?

A

IL-4 (mast cells produce these)

64
Q

Which clinical issues arise with elevated Th2 responses?

A

Th2 responses lead to IL-4 production which leads to IgE which causes type I sensitivity disorders

65
Q

What are cytokines?

A

Small proteins/glycoproteins that act via specific receptors - can be inflammatory or anti-inflammatory

66
Q

Define ‘pleiotropy’

A

Can have multiple effects

67
Q

What are the 4 attributes of cytokines?

A

can have multiple effects, different cytokines can do same job, can work together to cause effect, can have opposing effect

68
Q

Define autocrine transmission

A

Same cell is target that produced it

69
Q

Define paracrine transmission

A

Target cell is nearby to producing cell

70
Q

Define endocrine transmission

A

Target cell is distant and molecule travels in circulation

71
Q

What are chemokines?

A

Subfamily of cytokines involved in cellular movement (cells migrate towards high concentration); they signal through GPCR

72
Q

Describe the function of cytokines in inflammation

A

Macrophages at site of injury/infection –> inflammatory response –> TNF-alpha cytokine and chemokines –> TNF-a increases adhesion molecules and chemokines also activate adhesion molecules to bind to innate cells (neutrophils and monocytes) –> IL-2 cytokine drives T cell proliferation later

73
Q

When are cytokines pathological?

A

If there is uncontrolled systemic TNF-a –> septic shock.

Cytokine production uncontrolled –> more and more cytokine in positive feedback (Ebola)

74
Q

What is involved in type 1 hypersensitivity disorders?

A

Over-production of IL-3 causes overproduction of Th2 cells –> mast cell degranulation

75
Q

What is involved in chronic inflammation?

A

Over-production of Th1 cytokines –> chronic inflammation e.g. Chrohn’s

76
Q

How may inflammatory conditions be treated?

A

Anti-TNFa therapy

FUNMED (8 decks)

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