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MedST IB: Biology of Disease (BoD) > 1.0 Immunology > Flashcards

1.0 Immunology Flashcards

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1
Q

What occurs in reversible injury?

A

1) Cell swelling<br></br>2) Fatty deposits

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2
Q

Apoptosis vs necrosis

A

“<div><img></img></div>”

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3
Q

Humoral vs cellular immunity

A

<b>Humoral</b> - antibody/complement mediated immunity<br></br><b>Cellular</b> - T cells (+ cytokine release)

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4
Q

Innate vs adaptive immunity

A

“<div><img></img></div>”

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5
Q

What is the main haematopoietic organ?

A

Bone marrow

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6
Q

What are the primary lymphoid organs?

A

1) Bone marrow<br></br>2) Thymus

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7
Q

What are the secondary lymphoid organs?

A

1) Lymph node<br></br>2) Spleen

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8
Q

What are some lymphoid tissues?

A

1) Intestine<br></br>2) Tonsils (+ other mucous membranes)<br></br>3) Skin<br></br>4) Blood + lymph

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9
Q

What immune cells are lymphoid derived?

A

1) NK cells<br></br>2) B + T lymphocytes

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10
Q

What immune cells are myeloid derived?

A

<b>Granulocytes</b><br></br>1) Neutrophils<br></br>2) Eosinophils<br></br>3) Basophils<br></br>4) Mast cells<br></br><br></br><b>Monocytes</b><br></br><br></br><b>Macrophages</b>

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11
Q

What cells are the following CD proteins found on? (also what is their function?):<br></br><br></br>CD3<br></br>CD4<br></br>CD8<br></br>CD16<br></br>CD19<br></br>CD45<br></br>CD56

A

“<div><img></img></div>”

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12
Q

What concentrations do cytokines work at?

A

10⁻¹⁰ - 10⁻¹⁵ M

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13
Q

Name four families of cytokines:

A

1) Interleukins<br></br>2) Chemokines<br></br>3) TNF<br></br>4) Interferons

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14
Q

What characteristics do all cytokines share?

A

1) Pleiotropism<br></br>2) Redundancy<br></br>3) Antagonism<br></br>4) Synergism

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15
Q

What is FAS ligand?

A

(FasL/CD95)<br></br>Member of TNF family<br></br>Trimer that binds to FAS receptor (CD95)<br></br>Causes apoptosis

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16
Q

What is perforin?

A

Monomer (similar to C9)<br></br>Aggregates → forms pores → allows ingress of <b>granzymes</b> → starts caspase cascade

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17
Q

What are the three kinds of innate immune recognition?

A

1) PAMPs<br></br>2) DAMPs<br></br>3) Missing self

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18
Q

What are the characteristics of PAMPs?

A

1) Shared by different organism classes<br></br>2) Molecular constituents essential for survival<br></br>3) Highly conserved<br></br>4) Not present in vertebral hosts<br></br>5) Allow discrimination between self and non-self

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19
Q

Give examples of PAMPs for:<br></br>1) Bacteria<br></br>2) Yeast<br></br>3) Viruses<br></br>4) Parasites

A

“<div><img></img></div>”

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20
Q

Give 5 examples of PRRs:

A

1) Toll-like receptors (TLRs)<br></br>2) Lectins + scavenger proteins (MBL)<br></br>3) NOD + NOD-like receptors (NLRs)<br></br>4) RIG-like receptors (RLRs)<br></br>5) DNA receptors<br></br>6) Others (CRP)

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21
Q

What happens on activation of TLRs?

A

Activation → cytokine release → inflammation<br></br><br></br>Signal is via TIR domains<br></br>Activate NFkB, AP1 and IRF3 transcription factors

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22
Q

What are the ligands for the different TLRs?

A

“<div><img></img></div>”

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23
Q

What is the mechanism of TLR4 action?

A

“<div><img></img></div>”

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24
Q

How many types of NLRs are there in humans?

A

22

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25
Q

Where are NLRs located?

A

Cytoplasm

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26
Q

What are two subfamilies of NLRs?

A

1) NOD subfamily<br></br>2) NLRP subfamily

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27
Q

What do the NOD subfamily (of NLRs) cause on activation?

A

Activation → NFkB → inflammation

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28
Q

What proteins form the inflammasome complex?

A

1) NALP3<br></br>2) Caspase 1<br></br>3) ASC

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29
Q

Mechanism of inflammasome action:

A

1) PAMP is recognised → complex formation<br></br>2) NALP3 activates caspase 1<br></br>3) Caspase 1 converts proIL-1β → IL-1β<br></br><br></br>IL-1β promotes inflammation

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30
Q

What are DAMPs?

A

Danger associated molecular pathogens<br></br><br></br>Molecules that initiate non-infectious immune response<br></br>Normal tissue can cause immune response if damaged by trauma/infection

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31
Q

Examples of DAMPs:

A

<b>1) Intracellular proteins</b><br></br>- Heat shock protein<br></br>- HMGB1<br></br><b>2) Intracellular molecules</b><br></br>- ATP<br></br>- Uric acid<br></br>- DNA/RNA<br></br><b>3) Extracellular molecules</b><br></br><b>4) Non-self irritants</b><br></br>- Aluminium<br></br>- Silica

32
Q

What are the steps for neutrophil killing of pathogens?

A

1) Bacteria is phagocytosed<br></br>2) Phagosome fuses with granules from cytosol<br></br>3) pH of phagosome ↑ → killing bacteria<br></br>4) pF of phagosome ↓ → fusion with lysosome → complete degradation of bacterium<br></br>5) Neutrophil dies by apoptosis and is phagocytosed by macrophage

33
Q

What is the 2 receptor hypothesis of NK cells?

A

They have two receptors:<br></br>1) Activating receptor<br></br>2) MHC I inhibitory receptor<br></br><br></br>Presence of ligand at both → no killing<br></br>Presence of activatory ligand + absence of MHC 1 → killing of cell

34
Q

What are the two types of interferon?

A

<b>Type 1 = IFN α + β</b><br></br>Produced by cells with viral infections<br></br>These interferons interfere with viral replication and alert neighbouring cells and activate NK cells<br></br><br></br><b>Type 2 = IFN γ</b><br></br>Produced by activated NK cells<br></br>Activate macrophages

35
Q

What are the characteristics of acute inflammation? (cardinal signs)

A

1) Dolor (pain)<br></br>2) Calor (temp)<br></br>3) Rubor (redness)<br></br>4) Tumor (swelling)<br></br>5) Functio laesa (loss of function)

36
Q

Name 3 resident immune cells (resident in tissues):

A

1) Macrophages<br></br>2) Dendritic cells<br></br>3) Mast cells

37
Q

Local enzyme cascades contribute to inflammation. What do the following cascade products cause?<br></br>1) Bradykinin<br></br>2) Fibrin clot<br></br>3) Plasmin

A

<b>1) Bradykinin</b><br></br>- Vasodilation<br></br>- ↑ vascular permeability<br></br>- Pain<br></br><br></br><b>2) Fibrin clot</b><br></br>- Prevents spread of infection<br></br><br></br><b>3) Plasmin</b><br></br>- Breaks down clot<br></br>- Activates complement

38
Q

What effect do the following cytokines have?<br></br>1) IL-1α + IL-1β<br></br>2) IL-6<br></br>3) IL-12<br></br>4) TNFα<br></br>5) CXCL8 (IL-8)

A

<b>1) IL-1α + IL-1β</b><br></br>- Pro-inflammatory<br></br>- Endogenous pyrogen (fever)<br></br><br></br><b>2) IL-6</b><br></br>- Pro-inflammatory<br></br>- Endogenous pyrogen (fever)<br></br>- Stimulates acute phase proteins<br></br><br></br><b>3) IL-12</b><br></br>- Stimulates NK + T cells → <br></br>i) ↑ IFN γ and TNFα secretion<br></br>ii) ↑ cytotoxicity<br></br>iii) ↑ Differentiation into Th1<br></br><br></br><b>4) TNFα</b><br></br>- Stimulates acute phase proteins<br></br>- Endogenous pyrogen (fever)<br></br><br></br><b>5) CXCL8 (IL-8)</b><br></br>- Attracts neutrophils

39
Q

What are the acute phase protiens?

A

“<div><img></img></div>”

40
Q

Activated endothelial cells make ligands to L-selectin and integrin. What do they do?

A

<b>L-selectin</b><br></br>This is a lectin that binds carbohydrates<br></br>Allows rolling and slowing down of cell<br></br><br></br><b>Integrin</b><br></br>This is an adhesion molecule (binds to ICAM-1)<br></br>Allows cell to stop, adhere and transmigrate

41
Q

Compare + contrast neutrophils and macrophages:

A

“<div><img></img></div>”

42
Q

What factors lead to the termination of inflammation?

A

1) Inflammaotry <b>mediators are short lived</b> (↓ 1/2 life)<br></br>2) Macrophages secrete <b>TGFβ</b> → ↓ inflamm.<br></br>3) <b>IL-10</b> (from monocytes) → ↓ inflamm.<br></br>4) <b>Lipoxins</b> (from arachidonic acid) → ↓ inflamm.<br></br>5) <b>IL-1R antagonist</b><br></br>6) Pro-inflamm. <b>cells die by apoptosis</b>

43
Q

What cell plays a key role in tissue repair?

A

Macrophages (M2)

44
Q

What is a granuloma?

A

Walls off persistent pathogen<br></br>May have necrotic core<br></br>Lost of <b>macrophages</b> (histioctytes) - may fuse to become <b>giant cells</b> (multinucleated)<br></br>Granuloma is surrounded by:<br></br>1) Epitheloid macrophages (shoe sole shaped nuclei)<br></br>2) ECM (collagen)<br></br>3) other cells (lymphocytes, neutrophils + fibroblasts)

45
Q

What are the three main functions of the complement system?

A

1) Activate inflamamtion<br></br>2) Opsonisation<br></br>3) Lysis of target cells

46
Q

What is the bond present in C3?

A

Internal <b>thioester bond</b>

47
Q

Compare and contrast C3a + C3b:

A

<b>C3a</b><br></br>Small<br></br>Causes anaphylaxis<br></br>Activates/recruits phagocytes<br></br><br></br><b>C3b</b><br></br>Larger<br></br>Thioester bond<br></br>Susceptible to nucelophilic attack

48
Q

What factors regulate C3bBb complex?<br></br>(including factors that allow host cells to escape complement activation)

A

<b>Activated by</b><br></br>Properdin (Factor P)<br></br><br></br><b>Inhibited by</b><br></br>Factor H<br></br>Factor I<br></br>DAF<br></br>MCP

49
Q

What is the membrane attack complex?

A

C5a,6,7,8,9

50
Q

What bacterial diseases require MAC for clearance?

A

Useful for Gram -ve<br></br>Especially Neiserria (gonorrhea + Neisseria)

51
Q

How does the host cell escape MAC?

A

CD59 prevents pore formation

52
Q

What do C3a and C5a cause?

A

Anaphylaxis<br></br>C5a also recruits neutrophils

53
Q

What are the steps of the lectin pathway?

A

MBL + MASP-1 + MASP-2<br></br>MASP-2 : C4 to C4a + C4b<br></br>C4b: C2 to C2a + C2b<br></br>C4bC2a = Classic convertase (Converts C3 to C3a + C3b)

54
Q

What does mannose-binding lectin (MBL) bind to?

A

Mannose + Fructose

55
Q

What are the steps of the classical pathway?

A

CRP binds to phosphocholine<br></br>Recruits C1<br></br>Results in cleavage of C4 - C4a + C4b

56
Q

What is C1 composed of?

A

C1q x 6 (binds to IgG + IgM)<br></br>C1r (serine protease)<br></br>C1s (seine protease)

57
Q

What are the three ways in which antibodies work?

A

1) Neutralisation<br></br>2) Opsonisation<br></br>3) Complement activation

58
Q

Which organ does B cell rearrange its receptors?

A

Bone marrow

59
Q

Which organ does T cell rearrange its receptors?

A

Thymus

60
Q

Where are naive cells activated?

A

Secondary lymphoid tissue (lymph node + spleen)

61
Q

What type of bond joins the light and heavy chains in antibodies?

A

Disulphide bridge (covalent bond)

62
Q

What provides variation in antigen binding site?

A

Complimentary determining regions (CDRs)

63
Q

How many constant + variable domains are there in light and heavy chains?

A

<b>Light chain</b><br></br>1 x constant<br></br>1 x variable<br></br><br></br><b>Heavy chain</b><br></br>1 x variable<br></br>3 x constant (IgA, IgG, IgD) or 4 x constant (IgM, IgE)

64
Q

What does the hinge region in the antibody provide?

A

Flexibility

65
Q

What four main processes generate antibody diversity?

A

1) Different heavy and light chain combinations<br></br>2) Selection of different V, D, J segments<br></br>3) Junctional diversity<br></br>4) Somatic hypermutation

66
Q

What BCR isotype do all naive B cells have?

A

IgM

67
Q

What receptor mediates ADCC?

A

FcγRIII (IgG-NK cell interaction)<br></br><br></br>(also FcεRI mediates IgE-Eosinophil interactions)

68
Q

What receptors are on mast cells and cause degranulation?

A

FcγRIII + FcεRI

69
Q

How are antibody responses terminated?

A

-ve feedback (B cells have FcγRIIb to create -ve feedback loop)

70
Q

Define affinity:

A

Interaction between single Ab binding site and a single monovalent epitope

71
Q

Define avidity:

A

Measure of strength of interaction. Accounts for polyvalent epitopes

72
Q

Compare and contrast MHC class I and II structures and binding grooves:

A

“<div><img></img></div>”

73
Q

What is the length of peptides that MHC I and MHC II can bind?

A

MHC I = 8-9 peptides long<br></br><br></br>MHC II = 13-25 peptides long

74
Q

What are the different MHC class I isotypes?<br></br><br></br>What are the different MHC class II isotypes?

A

<b>Class I</b><br></br>HLA-A , HLA-B, HLA-C<br></br><br></br><b>Class II</b><br></br>HLA-DP, HLA-DQ, HLA-DR

75
Q

What is MHC restriction?

A

TCR sees part of both the MHC molecule and the peptide, therefore the TCR can’t respond to a peptide that is presented by a different MHC

76
Q

What are T-cells selected for?

A

1) β chain maturation<br></br>2) Positive selection<br></br>2) Negative selection

MedST IB: Biology of Disease (BoD) (9 decks)

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