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Y1S1- Fundamentals of Medicine > Immunity > Flashcards

Immunity Flashcards

1
Q

immune molecules that mediate immune responses

A

complement, cytokines and antibodies

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2
Q

cytokines

A

immune messenger hormones (IFNs, ILs, TGFs and chemokines which are chemoattractants)

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3
Q

complement cascade

A

sequence of soluble blood proteins/ enzymes that are cleaved downstream, 3 pathways by which it can be stimulated, all of which converge at the stage producing the enzyme C3 convertase, which cleaves the protein C3 into C3a and C3b.

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4
Q

myeloid immune cells

A
  • Neutrophils
  • Monocytes
  • Macrophages
  • Mast cells (in tissue)
  • basophils (in blood)
  • eosinophils
    [part of innate immune system]
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5
Q

lymphocytes

A
  • T lymphocytes
  • B lymphocytes
  • Plasma cells
  • Natural killer cells
    [mainly part of adaptive immune system- apart from NKCs]
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6
Q

neutrophils

A

most abundant, good at killing, recruited rapidly to the scene, very short lived, chief constituent of pus, IL-8 stimulate their production in bone marrow

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7
Q

non-phagocytic immune cells

A

basophils and mast cells

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8
Q

why do mast cells and basophils release heparin and histamine from granules?

A

causes vasodilation

[mainly part of innate immune system]

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9
Q

macrophages

A

good at killing if activated, reside in tissue, involved in tissue healing, clearance of dead cells & metabolism

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10
Q

which immune cells are involved in allergic and anti-parasitic reactions?

A

Mast cells (in tissue), basophils (in blood), eosinophils

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11
Q

C3a (anaphlatoxin) function

A

increases the inflammatory response, stimulating mast cell degredation

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12
Q

C3b function

A

acts as an opsonin on cells

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13
Q

C5b function

A

along with other cascade products produces a membrane attack complex (MAC), this forms a small pore in the membrane of a pathogen so water rushes in and ions out, leading to lysis which kills the cell

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14
Q

classical pathway of complement activation

A

only occurs when there are antibodies present specific to foreign antigen

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15
Q

mannose binding lectin pathway of complement activation

A

activation through binding of mannose (or similar carbohydrates) by mannose binding lectin on bacteria

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16
Q

alternative pathway of complement activation

A

complement component C3 is spontaneously activated and binds to nearby membranes and bacteria to activate complement as they lack control proteins on surface to prevent activation

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17
Q

types of T lymphocytes

A
  • Cytotoxic T cells (CD8+ T cells) kill infected or mutated cells
  • Helper T cells (CD4+ T cells) produce cytokines for other cells to respond to, organises body’s immune response
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18
Q

NK cells

A

provoke apoptosis in cells missing MHC I markers

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19
Q

plasma cells

A

activated B lymphocytes, produce antibodies

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20
Q

where are T cells made?

A

thymus

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21
Q

where are B cells made?

A

bone marrow and then mature further in spleen

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22
Q

primary lymphoid organs

A

bone marrow and thymus

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23
Q

secondary lymphoid organs

A

lymph nodes, spleen, tonsils, Peter’s patches in gut

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24
Q

maturation of B cells in bone marrow

A

Hematopoietic stem cells → pro B cells → pre B cells → immature B cell

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25
Q

what do lymphatic vessels drain into?

A

the lymph nodes at the junctions where the adaptive immune system scans the fluid for pathogens and initiates a response if necessary

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26
Q

what does the lymphatic system drain into?

A

the blood via the thoracic duct

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27
Q

thymus

A

gland between the sternum and lungs that is only active until puberty after which it begins to shrink and become replaced by fat

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28
Q

what are leukocytes derived from?

A

bone marrow stem cells

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29
Q

where are B cells located

A

lymphoid follicles

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30
Q

how do T and B cells enter and leave lymph nodes?

A

via blood vessels and leave via efferent lymphatic vessels found in the central medullary region

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31
Q

APCs

A

antigen presenting cells,

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32
Q

how do naive CD4 helper T cells mature?

A

APCs present antigens to them via MHC Class 2, this binding triggers maturation and stimulated cytokine release

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33
Q

types of APC

A

dendritic cell (main), macrophage, B cell

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34
Q

first line of defence in immune response

A

are physical barriers like skin, epithelia and mucous membranes

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35
Q

MHC (major histocompatibility complex)

A

a protein coded for by the human leukocyte antigen (HLA) gene and located on chromosome 6
General function- presenting antigens to adaptive immune system.

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36
Q

MHC Class 1

A

found on all nucleated cells apart from neurons, presents endogenous antigens (antigens within host cells) to cytotoxic T cells

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37
Q

how do NK cells recognise and kill viral cells?

A

viruses downregulate production of MHC Class 1 so NK cells bind to the cells and kill it via apoptosis

38
Q

what prevents NK cells from killing every cell?

A

inhibitory receptors that bind to MHC Class 1

39
Q

innate immune system

A
  1. Infection or necrosis releases PAMP and DAMP signals and also activates basophils, mast cells and resident macrophages- non-specific phagocytes fully activated by IFNy from other macrophages, NKs or T-helper cells
  2. These signals bind to PRRs (toll like receptors, C-type lectins or nod like receptors) on phagocytes, stimulating chemotaxis of neutrophils and releasing inflammatory mediators (cytokines)- IFNs, ILs, TNFs and kinins
  3. Neutrophils phagocytose debris/pathogens and IL-8 stimulates their production in bone marrow, pseudopodia extend around the pathogen to meet it in a phagosome, this fuses with a lysosome to give a phagolysosome which actively pumps in H ions to activate acid proteases such cathepsins
  4. PAMPs and DAMPs activate the complement cascade causing extravasation, opsonisation and MACs
  5. Use of NETs on parasites/fungi as a last resort
40
Q

2 components of acquired immune response

A

humoral (B cells) in fluid and cell mediated (T cells) in tissues

41
Q

epitope

A

part of antigen that immune cell recognises

42
Q

what do linear T cells recognise?

A

proteins so must have the antigen presented to them

43
Q

B cell recognition

A

B cells recognise soluble antigens in fluid and produce antibodies to clump the pathogen, to prevent binding to host receptors which would allow entry to host cells

44
Q

BCR structure

A

Y shaped receptor with a heavy chain and 2 light chains with variable regions with antigen binding sites on the end of light chains.

45
Q

TCR structure

A

alpha chain and a beta chains with antigen binding sites at the end of both chains

46
Q

somatic hypermutations

A

When a B cell is activated, it proliferates and during this it undergoes a high rate of mutation → largely driven by substitutions of single bases in the heavy chain of the BCR and variable V region of light chain

47
Q

junctional diversity

A

extra/fewer nucleotides at VDJ regions

48
Q

combinatorial diversity

A

different combos of V,D,J
BCR- difference combinations of heavy and light chains
TCR- different combos of alpha and beta chains

49
Q

somatic recombination

A

random pairing of V, D and J regions in BCRs and TCRs

50
Q

negative selection in B cell development

A

B cells that react too strongly to self antigens are deleted

51
Q

positive T cell selection

A

any lymphocyte which bind weakly to MHC molecules undergo apoptosis which ensures all T cells can recognise MHCs

52
Q

negative T cell selection

A

medullary dendritic and epithelial cells present self-antigens to lymphocyte and those which bind strongly to them are forced to undergo apoptosis

53
Q

MHC Class 2

A

present on specialised APCs only, present endogenous antigens by CD4 (helper) lymphocytes

54
Q

what do TI IFNs produced by NK cells do?

A

message an anti-viral state to nearby cells- prevents viral proliferation

55
Q

what do specialised APCs do?

A

take up the antigen, present it on an Class II MHC and upregulate cytokine production. They drain into the lymphatics and present to CH4 (helper) cells in the lymph nodes (call this signal 1).

56
Q

signal 2

A

CD4 cells then send a co-stimulatory signal back to APCs, signifies them recognising the foreign antigen and allows immune response

57
Q

why do CD4s release cytokines?

A

to direct B cells, CD8s and APCs

58
Q

how to CD8s induce apoptosis in infected cells?

A

them using the Fas death ligand or perforin and granzyme- both stimulate caspase cascade

59
Q

why are memory T cells produced?

A

to mount a faster 2nd response if re-infection occurs

60
Q

humoral immunity

A

BCRs complementary to a specific antigen detect it and present it on a Class II MHC. Co-stimulation form activated T helper cells activates the B cells which divide to produce many clones. These either differentiate into plasma cells (also called immunoglobulins)- produce antibodies or memory cells which remain in the bloodstream long after infection so that the 2nd response is faster if the pathogen re-enters, antibodies can also activate complements

61
Q

T cell immunity compared to humoural immunity

A

antibodies can be generated directly after antigen detection response will be faster but less effective

62
Q

immunoglobulin types

A

IgM, IgA, IgD, IgE, IgG

63
Q

IgA

A
  • Fc alpha
  • Dimer
  • Neutralisation and flushing mucosal pathogens
  • Most abundant in mucosal tissues
64
Q

IgD

A
  • Monomer
65
Q

IgE

A
  • monomer
  • mast cell, basophils and eosinophil activation in allergy
  • on surface of mast cells
  • deals with allergy reactions and dealing with helminths
66
Q

IgG

A
  • monomer
  • neutralisation
  • opsonises pathogens or phagocytosis
  • complement activation
  • ADCC
  • Can cross placenta
  • Abundant in extra-mucosal tissues
  • Four subclasses: IgG1, IgG2, IgG3, IgG4
67
Q

IgM

A
  • pentamer
  • first to be released and not very specific
  • neutralisation
  • complement activation
  • primarily in blood
68
Q

ADCC (antibody dependant cell mediated cytotoxicity)

A

antibodies bind to surface antigen presented by an infected cell (opsonisation without phagocytosis), NKs and neutrophils release cytotoxic granules containing perforin, granzyme and TNFalpha which induced apoptosis in a cell

69
Q

class switching

A

T cell signals to activated B cell to produce a different class of antibody (probably be CD40L from the helper T cell binding to the CD40 receptor on the B cell), the B cell will produce IgM first but will undergo gene rearrangement ot produce a different one (IgG, IgA or IgE)

70
Q

why can’t class switching occur in T independent activation?

A

only IgM will be produced

71
Q

affinity maturation

A

helper T cells select those activated B cells which have been mutated to produce antibodies with the highest affinity for an antigen to survive as a plasma cell or memory B cell, lower affinity ones are rejected and die

72
Q

T independant activation

A

the additional signals will come from microbes, cytokines and APCs. This activation will cause the B cell to produce IgM

73
Q

what is T cell dependant activation in response to?

A

protein antigens like viral proteins which bind to BCRs and allow them to get degraded by lysosomes. The peptides from the internal proteins of the virus are exposed and can be loaded onto MHC Class II to be presented on the B cell surface. At this point a helper T cell will recognise the presented peptide via it’s TCR and provide co-stimulation to the B cell.

74
Q

what enzyme plays a role in somatic hypermutation and class switching?

A

activation-induced cytidine deaminase

75
Q

Type 1- IgE mediated hypersensitivity mechanism

A

Ag induces induces cross- linking of IgE bound to mast cells with release of vasoactive mediators
Symptoms:
- Vasodilation due to histamine ect. - hypotension, oedema
- Bronchoconstriction (histamine, bradykinins)
Treatment is symptomatic: adrenaline, beta agonists, IV fluids, corticosteroids

76
Q

examples of type 1 hypersensitivity

A

[anaphylaxis], hay fever, eczema

77
Q

type 2- Ab-mediated cytotoxic hypersensitivity

A

Ab directed to cell surface IgG or IgM mediates destruction by phagocytosis, ADCC or complement-mediated lysis

78
Q

type 3- immune complex mediated hypersensitivity

A

IgG/M complexes induce mast cell degranulation via FcgRIII

79
Q

type 2 hypersensitivity examples

A

Blood transfusion reactions, Rhesus reactions, Graves disease, myasthenia gravis

80
Q

type 3 hypersensitivity examples

A

Arthus reaction, Serum reaction, systemic lupus erythematosus

81
Q

type 4- T cell mediated hypersensitivity

A

Delayed type, TH1 cells release cytokines that recruit and activate macrophages

82
Q

type 4 hypersensitivity examples

A

Tubercular lesions, contact dermatitis

83
Q

autoimmunity

A

type II, immunity misdirected at healthy tissues,

characteristics: chronic disease with relapse & remission, clinical symptoms shaped by nature of immune response

84
Q

Genes for MHC Class 1

A

A/B/C

85
Q

genes for MHC class 2

A

DP/DQ/DR

86
Q

regions in BCRs

A

light chain= VJ

heavy chain= VDJ

87
Q

regions in TCRs

A

alpha chain= VJ

beta chain= VDJ

88
Q

peripheral tolerance

A

Activation of lymphocytes requires multiple signals or cells become anergic

89
Q

immune regulation by

A

T-regulatory cells (Tregs)

90
Q

central tolerance

A
  • Deletion of self reactive T cells in the thymus

- Deletion of self reactive B cells in the bone marrow

Y1S1- Fundamentals of Medicine (11 decks)

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