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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
IL-12 (pro-lnf)
activates NK cells CD4 -> Th1
26
TNF-a (pro-inf)
activate vascular endothelium | inc vascular permeability
27
acute phase proteins (markers of inflammation)
IL-1, IL-6, TNF-a -> made in the LIVER -> CRP (c-reactive proteins) & mannose-binding lectin -> activation of complement system
28
licenced DCs go back to the lymph node
TNF-a stimulates migration of DC to LN and maturation -> initiation of adaptive immune response
29
acute phase response (markers of inflammation)
``` MAJOR: (serum) amyloid A & CRP complements coag proteins protease inhibitors METAL-BINDING proteins ```
30
viral response
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
31
cytokines that activate NK cells
IL-12 | IFN-a,b
32
how cells w/ MHC I provide negative signal to NK cells
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
gamma:delta T cells
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
plasmacytoid dendritic cell
innate immunity sentinels fro virus infection makes IFN-a,b makes CD40Ligand to bind to CD40 on CDC
35
moderate affinity IL-2 receptors high affinity IL-2 receptors (activated by IL-12 from APCs)
moderate: IL-2R BETA & GAMMA high: IL-2R ALPHA, beta, gamma
36
CTLA4
receptor on activate T cell that binds more strongly to B7 (than CD28 on APC) down-regulate Tcell proliferation
37
only activated, effector CD8 only need signal 1 TCR:MHC+Ag to kill the infected cells
don't need co-stimulatory signal
38
granules released by CD8 & NK cells
perforin granzymes (serine protease that activate apoptosis) granu-lysin (antimicrobial actions, induces apoptosis)
39
most CD8 cell responses require CD4 T cells
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
Th17
makes (IL-17)-> fibroblasts, epithelial cells -(chemokines)-> neutrophils enhance neut response promote barrier integrity (skin, intestine) k. pneumoniae, fungi (candida albicans)
41
what cytokine ups Th1 and inhibits Th2? | what cytokine ups Th2 and inhibits Th1?
IFN-gamma inhibits Th2 IDO (indoleamine dioxygenase) toxic for Th1
42
when a naive T cell that escaped the thymus bind to self-Ag on epithelial cell, only get signal 1 -> anergy
eg. generally mucosal DCs (poorly licensed DCs) induce Treg in the absence of inflammatory stimuli
43
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)
.
44
Ig production against LIPID antigens; mediated by what kind of APC and T cell?
DC loads lipid molecule on CD1d -> iNK T cell -> B cell IgG, little affinity maturation, no memory cells
45
NK cells that have Fc receptors can kill Ig-coated target cells via _______
ADCC (antibody dependent cellular cytotoxicity)
46
eosinophil & mast cells have receptors for which Ig's?
IgA AND IgG
47
mast cell, which Ig?
IgE
48
RAST (radio-allergo-sorbent test) assay
measure HOW MUCH IgE there is to be specific allergen (in vitro) need: insolubilized allergen + pt's serum w/ IgE + radiolabeled anti-IgE
49
which part of the Precipitating Curve is the SOLUBLE IMMUNE COMPLEX (type 3) most likely to form
antigen excess
50
Type 3: SERUM SICKNESS - generalized or localized?
``` aka. transient immune complex-mediated syndrome generalized cause: drug rxn (penicilin) erythematous rash, lymphadenopathy fever, vasculitis, arthritis, nephritis ```
51
Type 3: ARTHUS REACTION - generalized or localized?
localized | IgG
52
mechanism of Anti-histamine
competitively blocks histamine binding sites in upper airways (nose) & skin
53
mechanism of Cromolyn Sodium
inhibit mast cell degranulation | administration: inhalation
54
Desensitization shot/hyposensitization therapy:
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
skin test
have pts wait 30 min; can release after 30 min | start w/ very dilute Ag (1:100) → if (-) result, try 1:10 dilution
56
Ragweed pollenosis = allergic rhinitis = hay fever
eyes and nose
57
capsule is made out of _______ and looks like host connective tissue, so it's not targeted
hyaluronic acid
58
bacterial adhesions
``` fimbrial M protein Lipoteichoic acids (LTA) ```
59
what bacterial component is the primary target for antibodies
Fimbrial M
60
Rheumatic fever
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
Acute Glomerulonephritis: Ig made against what bacterial component
type 3 | DNAse B
62
immunologically privileged sites
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
regulatory or infectious tolerance
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
which receptor allows inappropriate crosslinking of Igs by self-DNA in B cells
TLR-9 self DNA: unmethylated dsDNA in chronic inflammation/necrosis (massive cell death or inflammation)
65
Guillian-Barre (molecular mimicry, autoimmune)
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
Grave's Disease (type 2)
plasma cells make Igs that act as TSH receptor on thyroid -> excessive TH production inappropriate expression of MHC II on thyroid acinar cells
67
Myasthenia Gravis
Ig binds to AchR on NMJ w/o activation
68
inappropriate expression of MHC II in autoimmune disease
on pancreatic b cells in insulin-dependent diabetes Graves' disease: on thyroid acinar cells
69
Bystander effect
autoimmune damage drives more autoimmune damage as more self-antigen is released
70
Leukocyte adhesion deficiency (phagocyte disorder)
delayed separation of the umbilicus | neuts can't go to tissue -> no pus formation
71
Chediak-Higashi syndrome
partial albinism; peripheral neuropathy | defective lyososome
72
chronic granulomatous disease
Increased susceptibility to catalase positive organisms Negative Nitroblue tetrazolium dye reduction test No NADPH oxidase lost respiratory burst to kill intracellular organisms
73
IL-12 receptor deficiency
dec INF-gamma ->no granulomas | disseminated mycobacerial infection -> TB everywhere
74
Bruton | agamma-globulinemia
BTK (tyrosine kinase) defect -> block B cell maturation -> dec all Igs boys recurrent bacterial infection
75
what is measured when screening neonates for SCID in the blood?
TRECs (tcell receptor-excision circles)
76
Ataxia telangiectasia
defective DNA repair enzymes Cerebellar defects -> ataxia Spider angiomas IgA deficiency
77
Graft vs Host disease
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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