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Q1 > ACI > Flashcards

ACI Flashcards

1
Q

what’s the FIRST system that is activated when an microorganism breaches the BARRIER EPITHELIAL?

A

complement system

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2
Q

complement proteins

A

PLASMA proteins, inactive (zymogen), SERINE proteases

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3
Q

Recurrent bacterial infection (URT, middle ear, sinuses) in infant

A

defective neut adherence and chemotaxis; deficient in cell-associated glycoprotein

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4
Q

the AMPLIFICATION step in complement is mediated by what enzyme

A

convertases (c3 convertase, c5 convertase): cleaves c3 -> c3a, c3b

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5
Q

5 outcomes of complement activation

A 
opsonization of pathogens
recruit inflammatory cells 
B cell trigger/maturation, Tcell activity 
immune complex removal 
killing of pathogen
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6
Q

c1q binds to (3)

A

IgM, IgG
bacterial surface (directly)
C-reactive protein on bacterial surface

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7
Q

what part of Fc does the complement bind to?

for IgM and IgG

A

IgM: (two) CH3
IgG: CH2

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8
Q

which cells have c3a/c5a receptors; what does it activate inside the cell? what cells does it recruit once activated to the site of infection

A

PEM (phagocytes, endothelial cells, mast cells)
G-protein
RBCs (and other immune cells) to the site of infection

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9
Q

what complement protein (2nd signal) is needed for the phagocyte to engulf c3b coated bacteria?

A

c5a

don’t need it when the bacteria is coated w/ both c3b and IgG

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10
Q

which complement protein of the MAC complex inserts into the cell membrane?

A

c8

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11
Q

immune complex removal; RBC has which receptor that binds to which complement and takes to which organs to remove it?

A

c3b (on immune complex) binds to CR1 on RBCs and taken to spleen/liver

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12
Q

c1 (esterase) inhibitor - function?

deficiency?

A

prevent overactivation of complement system

hereditary angioedema
minor trauma to skin/mucosa triggers rapid, severe swelling that can obstruct the airway

c/i: ACE inhibitor

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13
Q

C3 deficiency

A

severe, recurrent bacterial infection (severe, recurrent pyogenic=pus sinus, resp tract infection)

inc susceptibility to type III hypersensitivity rxn - can’t remove immune complex w/o c3b

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14
Q

c5-c9 deficiencies (late steps) & alternative pathway (B,D)

A

recurrent NEISSERIAL infection

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15
Q

MBL deficiency in infants

A

recurrent bacterial infection (URT, etc. penumonia/meningitis)

pathogens w/ mannose & fucose

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16
Q

innate immunity features (key slide)

A

a primitive system conserved through evolution (inborne, not learned)
rapid response (min-hrs): use products of germ-line cells
not specifically directed against the invading pathogen (LOW specificity): recognizes PATTERNS - potential for collateral damage
vs. adaptive immunity: exquisite specificity minimizing collateral damage

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17
Q

Blood clotting: helps limit spread of infection

A

,

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18
Q

functions of normal microbiota (the microbiome) vs pathogenic bacteria

A
  1. maintains low but constant expression of MCHII on macrophages & other APCs
  2. stimulation of cross-protective antibodies (capsules of e.coli K1 & n. meningitidis are identical)
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19
Q

CD14 (PRR)

A

on Neut & Mac

receptors for LPS & LBP

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20
Q

what are the outcomes of PRR ligation? (key slide)

A

release of pro-inf cytokines
upregulation of chemokine receptors
*secretion of CCL18 to attract NAIVE Tcells
upregulation/expression of MHC 1& 2, co-stimulatory, cell adhesion molecules

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21
Q

gram (-) bacteria

A

LPS

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22
Q

gram (+) bacteria

A

c-reactive protein

phosphoryl-choline, phosphatidyl-lethanolamine

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23
Q

c-reactive protein

A

measured for sign of inflammation gram (+) cell wall

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24
Q

IL-1 (pro-inf)

A

activates vascular endothelium

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25
Q

IL-12 (pro-lnf)

A

activates NK cells

CD4 -> Th1

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26
Q

TNF-a (pro-inf)

A

activate vascular endothelium

inc vascular permeability

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27
Q

acute phase proteins (markers of inflammation)

A

IL-1, IL-6, TNF-a ->
made in the LIVER ->
CRP (c-reactive proteins) & mannose-binding lectin -> activation of complement system

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28
Q

licenced DCs go back to the lymph node

A

TNF-a stimulates migration of DC to LN and maturation -> initiation of adaptive immune response

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29
Q

acute phase response (markers of inflammation)

A 
MAJOR: (serum) amyloid A & CRP 
complements 
coag proteins 
protease inhibitors 
METAL-BINDING proteins
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30
Q

viral response

A

triggered by DOUBLE-STRANDED RNA (inside the virus-infected host cells) -> IFN-a,b ->
induce resistance to v rep in all cells
inc MHC I expression and Ag presentation in all cells
activate NK cells to kill virus-infected cells

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31
Q

cytokines that activate NK cells

A

IL-12

IFN-a,b

32
Q

how cells w/ MHC I provide negative signal to NK cells

A

KIR20/30 (killer inhibitory receptors) and CD94/NKG2 on NK cells bind to MHC1 -> inhibits signals from ‘NK-cell activating ligand’ -> NK cell doesn’t kill the normal cell

33
Q

gamma:delta T cells

A

in the germline sequence, innate cell
no memory function
no CD4/8
can recognize MIC (MHC class I like molecule) on infected epithelial cells
kills the infected epithelial cell -> helps repair the wound -> dead cells replaced by adjacent healthy cells

e.g. gut epithelial

34
Q

plasmacytoid dendritic cell

A

innate immunity
sentinels fro virus infection
makes IFN-a,b
makes CD40Ligand to bind to CD40 on CDC

35
Q

moderate affinity IL-2 receptors

high affinity IL-2 receptors (activated by IL-12 from APCs)

A

moderate: IL-2R BETA & GAMMA
high: IL-2R ALPHA, beta, gamma

36
Q

CTLA4

A

receptor on activate T cell that binds more strongly to B7 (than CD28 on APC)

down-regulate Tcell proliferation

37
Q

only activated, effector CD8 only need signal 1 TCR:MHC+Ag to kill the infected cells

A

don’t need co-stimulatory signal

38
Q

granules released by CD8 & NK cells

A

perforin
granzymes (serine protease that activate apoptosis)
granu-lysin (antimicrobial actions, induces apoptosis)

39
Q

most CD8 cell responses require CD4 T cells

A

via APC

APC increase CD40L to CD4

direct: CD4 release IL-2 to CD8
indirect via APC: make CD8 to increase expression of B7 & 4-IBB

40
Q

Th17

A

makes (IL-17)-> fibroblasts, epithelial cells -(chemokines)-> neutrophils

enhance neut response
promote barrier integrity (skin, intestine)

k. pneumoniae, fungi (candida albicans)

41
Q

what cytokine ups Th1 and inhibits Th2?

what cytokine ups Th2 and inhibits Th1?

A

IFN-gamma inhibits Th2

IDO (indoleamine dioxygenase) toxic for Th1

42
Q

when a naive T cell that escaped the thymus bind to self-Ag on epithelial cell, only get signal 1 -> anergy

A

eg. generally mucosal DCs (poorly licensed DCs) induce Treg in the absence of inflammatory stimuli

43
Q

during SECONDARY response, Ag-specific IgG suppresses the activation of naive B cells by cross-linking BCR + (inhibitory) Fc gamma RIIB1 on B-cell receptors to prevent its activation. and to activate a memory Bcell instead (make IgG/A/E)

A

.

44
Q

Ig production against LIPID antigens; mediated by what kind of APC and T cell?

A

DC loads lipid molecule on CD1d -> iNK T cell -> B cell

IgG, little affinity maturation, no memory cells

45
Q

NK cells that have Fc receptors can kill Ig-coated target cells via _______

A

ADCC (antibody dependent cellular cytotoxicity)

46
Q

eosinophil & mast cells have receptors for which Ig’s?

A

IgA AND IgG

47
Q

mast cell, which Ig?

A

IgE

48
Q

RAST (radio-allergo-sorbent test) assay

A

measure HOW MUCH IgE there is to be specific allergen (in vitro)
need: insolubilized allergen + pt’s serum w/ IgE + radiolabeled anti-IgE

49
Q

which part of the Precipitating Curve is the SOLUBLE IMMUNE COMPLEX (type 3) most likely to form

A

antigen excess

50
Q

Type 3: SERUM SICKNESS - generalized or localized?

A 
aka. transient immune complex-mediated syndrome 
generalized
cause: drug rxn (penicilin) 
erythematous rash, lymphadenopathy
fever, vasculitis, arthritis, nephritis
51
Q

Type 3: ARTHUS REACTION - generalized or localized?

A

localized

IgG

52
Q

mechanism of Anti-histamine

A

competitively blocks histamine binding sites in upper airways (nose) & skin

53
Q

mechanism of Cromolyn Sodium

A

inhibit mast cell degranulation

administration: inhalation

54
Q

Desensitization shot/hyposensitization therapy:

A

inc production of IgG “blocking antibody”, which binds to Ag before they can get to IgE+mast cells.
can be secretory IgA, too
takes mo to stimulate Ig production; small doses must be given initially to prevent induction of anaphylaxis and shots need to be repeated w/ increasing dose
1. inc production of IgG blocking antibody
2. [IgE] decreases as [IgG] increases over the months (mechanism unknown)
3. dec histamine release from sensitized mast cells
works better for insect venom sting than allergic rhinitis
insect venom sting: subQ -> lungs: has more opportunity to combine w/ serum IgG-blocking-antibody
allergic rhinitis: straight through nasal mucosa to submucosal mast cell, less exposure to IgG-blocking-antibody

55
Q

skin test

A

have pts wait 30 min; can release after 30 min

start w/ very dilute Ag (1:100) → if (-) result, try 1:10 dilution

56
Q

Ragweed pollenosis = allergic rhinitis = hay fever

A

eyes and nose

57
Q

capsule is made out of _______ and looks like host connective tissue, so it’s not targeted

A

hyaluronic acid

58
Q

bacterial adhesions

A 
fimbrial M protein 
Lipoteichoic acids (LTA)
59
Q

what bacterial component is the primary target for antibodies

A

Fimbrial M

60
Q

Rheumatic fever

A

Type 2 > 4
few wks after strep (group A) pharyngitis
Ig against STREPTOLYSIN O protein & same to against proteins in hearts/joints
Aschoff body: focal inflammatory lesion on the heart (macs and Tcells)

61
Q

Acute Glomerulonephritis: Ig made against what bacterial component

A

type 3

DNAse B

62
Q

immunologically privileged sites

A

brain, eyes, testes, uterus/fetus

fluid from these don’t pass through the lymphatics
barriers excludes naive lymphocytes
these sites express FAS ligand and induce apoptosis of Fas-bearing effector lymphocytes
Ags from these are accompanied by AI cytokines (TGF-b, IL-10)

63
Q

regulatory or infectious tolerance

A

Treg can suppress self-reactive lymphocytes even if they recognize DIFF epitopes, as long as they’re form the SAME TISSUE or Ag presented by the SAME APC

64
Q

which receptor allows inappropriate crosslinking of Igs by self-DNA in B cells

A

TLR-9
self DNA: unmethylated dsDNA

in chronic inflammation/necrosis (massive cell death or inflammation)

65
Q

Guillian-Barre (molecular mimicry, autoimmune)

A

self: peripheral nerve gnaglioside
Ag: Campylobacter jejuni (infection) or swine flu vaccine
s/s: actue paralysis
IR on axon, schwann cell surface, infiltration of nerve

66
Q

Grave’s Disease (type 2)

A

plasma cells make Igs that act as TSH receptor on thyroid -> excessive TH production

inappropriate expression of MHC II on thyroid acinar cells

67
Q

Myasthenia Gravis

A

Ig binds to AchR on NMJ w/o activation

68
Q

inappropriate expression of MHC II in autoimmune disease

A

on pancreatic b cells in insulin-dependent diabetes

Graves’ disease: on thyroid acinar cells

69
Q

Bystander effect

A

autoimmune damage drives more autoimmune damage as more self-antigen is released

70
Q

Leukocyte adhesion deficiency (phagocyte disorder)

A

delayed separation of the umbilicus

neuts can’t go to tissue -> no pus formation

71
Q

Chediak-Higashi syndrome

A

partial albinism; peripheral neuropathy

defective lyososome

72
Q

chronic granulomatous disease

A

Increased susceptibility to catalase positive organisms
Negative Nitroblue tetrazolium dye reduction test

No NADPH oxidase lost respiratory burst to kill intracellular organisms

73
Q

IL-12 receptor deficiency

A

dec INF-gamma ->no granulomas

disseminated mycobacerial infection -> TB everywhere

74
Q

Bruton

agamma-globulinemia

A

BTK (tyrosine kinase) defect -> block B cell maturation -> dec all Igs
boys
recurrent bacterial infection

75
Q

what is measured when screening neonates for SCID in the blood?

A

TRECs (tcell receptor-excision circles)

76
Q

Ataxia telangiectasia

A

defective DNA repair enzymes

Cerebellar defects -> ataxia
Spider angiomas
IgA deficiency

77
Q

Graft vs Host disease

A

BM transplant
target organs: skin(rash -> erythroderma) , gut (diarrhea), liver (bilirubin)

prevention

  1. partial tcell depletion of stem cell product (mature T cell causes the most of the damage)
  2. non-myeloablative protocol

pre-op tx: anti-lymphocytes anti-IL2R moab

Q1 (7 decks)

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