Immune system

Question 1

C3(H20)Bb

Answer 1

Fluid phase C3 convertase

Question 2

C3bBb

Answer 2

Alternative pathway C3 convertase

Question 3

C3b2Bb

Answer 3

Alternative pathway C5 convertase

Question 4

Mannose binding lectin

Answer 4

Soluble PRR that binds mannose and fucose residues on microbes
- Associated with MASP1/2 (serine proteases) that cleave C4 and C2

Question 5

C4bC2A

Answer 5

Classical C4 convertase

Question 6

C reactive protein

Answer 6

Soluble PRR that recognises phosphocholine on bacterial surfaces
Binds C1 and activates so C1s (serine protease part) can cleave C4 and C2

Question 7

Antibody inducing complement

Answer 7

Antibody binds C1q at Fc region causing conformational change to activate C1s/r
C1s can then cleave C4 and C2 to make classical C3 convertase

Question 8

C4bC2aC3b

Answer 8

Classical C5 convertase

Question 9

Factor P (properdin)

Answer 9

Stabilises C3 and C5 convertase (alternative) to assist MAC formation

Question 10

Factor I

Answer 10

Degrades C3b and C4b

Constitutively expressed

Question 11

Membrane cofactor protein (MCP)

Answer 11

Activates factor I (cofactor)

Dissociates classical and alternative C3 convertase via decay accelerating capacity

Question 12

Factor H

Answer 12

Cofactor for factor I but binds host sialic acid so specific

Question 13

Decay accelerating factor

Answer 13

Makes C3 convertases dissociate

On host

Question 14

Protectin

Answer 14

Prevents C9 recruitment so stops MAC

Question 15

FcgammaRIIIa

Answer 15

On NK cells to cause granule release for ADCC

And on mast cells for granule release

Question 16

FcgammaRIIb

Answer 16

-ve signal to turn off antibody response

Question 17

FcgammaRI

Answer 17

On macrophages for phagocytosis

Question 18

FcepsilonRI

Answer 18

On eosinophils to cause granules release to defend against helminths
On mast cells, often pretending IgE; cross linking causes degranulation in allergy

Question 19

IL-12

Answer 19

Activates NK cells

Causes naive T cells to become Th1

Question 20

Neutrophil recruitment sequence

Answer 20

s-Lex binds P selectin for weak tethering
LFA-1 binds ICAM-1; becomes tight when CXCL8 binds its receptor
LFA-1 interacts with CD31 for passage across tight junction
Follows CXCL8 gradient

Question 21

Granulation tissue

Answer 21

Macrophages are key
Fibroblasts recruited by FGF
Endothelial cells recruited by VEGF
Metalloproteinases from macrophages break down ECM for remodelling

Repair and inflammation at same time

Question 22

Master transcription factor for Th1, Th2, Th17, Treg

Answer 22

Th1 = T-bet
Th2 = GATA-3
Th17 = RORgammaT
Treg = FOXP3

Question 23

High vs low antigen dose

Answer 23

High dose -> Th1 response, high TCR affinity

Low dose -> Th2 response, low TCR affinity

Question 24

Anti-inflammatory cytokines

Answer 24

IL-10, TGF-beta

Question 25

Direct antibody autoimmunity

Answer 25

Graves disease: agonist at TSH receptor so hyperthyroidism Hashimoto's disease: anti-TSH so hypothyroidism Myasthenia Gravis: anti-nAChR so get paralysis and weakness

Question 26

Immune complex mediated autoimmunity

Answer 26

Systemic Lupus Erythematosus Autoantibodies against nuclear and cytoplasmic componenets Not cleared so deposit in kidneys, endothelium

Question 27

T cell mediated autoimmunity

Answer 27

Rheumatoid arthritis Multiple sclerosis Type 1 diabetes

Question 28

Type 1 hypersensitivity

Answer 28

Allergy IgE mediated Dendritic cell presents allergen to naive T cell in presence of IL-4 so get Th2 This release IL-4 and IL-13 to make B cell that produces IgE This gets rebound to receptors on mast cells which degranulate upon cross linking

Question 29

Type 2 hypersensitivity

Answer 29

IgM or IgE binding to cells and triggering clearance by macrophages/complement e.g in blood transfusion/rhesus antigen related

Question 30

To avoid rhesus antibody production

Answer 30

Add lots of anti-Rh antibodies to mask the presence of Rh antigens

Question 31

Type 3 hypersensitivity

Answer 31

IgG; immune complex deposition e.g serum sickness | Arthus reaction

Question 32

Type 4 hypersensitivity

Answer 32

T cell mediated | Haptens modify proteins causing their presentation and Th1 response

Question 33

Cytokines pro Th1

Answer 33

IL-1, IL-2, IL-12, TNF, IFNgamma

Question 34

Cytokines pro Th2

Answer 34

IL-4, IL-10, TGFbeta (anti-inflammatory)

Question 35

NOD like receptor mutation disease

Answer 35

Crohn's

Question 36

TLR4

Answer 36

LPS

Question 37

TLR5

Answer 37

Flagellin

Question 38

TLR 7 and 8

Answer 38

ssRNA

Question 39

TLR3

Answer 39

dsRNA

Question 40

RIG like receptors

Answer 40

Detect viral RNA in cytoplasm

Question 41

Macrophage produces

Answer 41

IL-1beta TNFalpha IL-6: lymphocyte activation, C reactive protein production CXCL8: chemokine to recruit neutrophils IL-12: activates NK cells and induces CD4 cells to become Th1

Question 42

Mast cell releases

Answer 42

Histamine, TNFalpha, leukotrienes, prostaglandins

Question 43

Vascular endothelium activation

Answer 43

Short term: by histamine; get P selection release from Weber Palade bodies Longer term: from IL-1 and TNFalpha get E selectin

Question 44

Monocyte recruitment adhesin molecule

Answer 44

VCAM-1

Question 45

Anti-inflammatory leukotriene

Answer 45

Lipoxin

Question 46

Anti-inflammatory cytokines

Answer 46

IL-10, TGFbeta

Question 47

Staphylococcus interaction with complement

Answer 47

Inhibits C3 convertases and degrades C3b

Question 48

Two signals to activate T cells

Answer 48

1) Via interaction of MHC with TCR | 2) Interaction of B7 (CD80/86 on B cell) with CD28

Question 49

Defective AIRE expression

Answer 49

Leads to APECED

Question 50

Lack of FoxP3

Answer 50

IPEX | X linked