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Microbiology/Immunology > innate immunity > Flashcards

innate immunity Flashcards

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Biology 101 flashcards
1
Q

effector functions of complement

A

opsonization and phagocytosis
leukocyte migration, chemotaxis, and inflammation
lysis of pathogens

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2
Q

classical complement pathway

A

initiated by antibody-antigen complexes
requires two IgG or one IgM attached to microbe
initiation component is C1
recognition component is C1qrs

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3
Q

alternative complement pathway

A

spontaneously activated

low level cleavage of C3 in plasma aka C3 tick-over –> generation of C3b –> C3b associates with microbial surface

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4
Q

lectin pathway

A

initiated by sugar residues on microbial surfaces that are not on host surfaces
initiation component is mannose binding lectin or ficolin in complex with MASP-1 or MASP-2

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5
Q

CD59

A

complement regulatory protein

prevents binding of C9 so that MAC cannot form

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6
Q

decay accelerating factor (DAF)

A

complement regulatory protein

dissociates C3 convertase so that C3 cannot be split into C3a and b

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7
Q

paroxysmal nocturnal hemoglobinuria

A

caused by deficiency of complement regulatory proteins

intravascular lysis of RBCs by complement

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8
Q

C1 inhibitor

A

binds activated C1r and C1s, dissociating them from C1q so that classical pathway cannot be activated

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9
Q

deficiency of C1 inhibitor

A

leads to HAE = hereditary angioneurotic edema (swelling of skin and larynx)

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10
Q

mechanisms by which complement regulatory proteins function

A

dissociate complement complexes

promote proteolysis of complement components

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11
Q

deficiency in early classical pathway components

A

immune complex disease (lupus)

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12
Q

deficiency in early lectin pathway components

A

increased susceptibility to bacterial infection

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13
Q

deficiency in early components of alternative pathway

A

increased susceptibility to infection with pyogenic bacteria and Neisseria

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14
Q

deficiency in C3 (all pathways)

A

increased susceptibility to infection with pyogenic bacteria and Neisseria

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15
Q

deficiency in terminal components of complement pathway (C5b-C9)

A

inability to generate MAC –> increased susceptibility to Neisseria infection

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16
Q

pro-inflammatory cytokines

A

TNF alpha, IL-1, IL-6

17
Q

antiviral state cytokines

A

interferons

18
Q

what PRR activates inflammasomes

A

NLRP, subfamily of NLRs

inflammasome then generates IL-1

19
Q

CD16

A

activates NK cells to kill virally infected cells by binding IgG that is bound to target cell

20
Q

how do NK cells kill by ADCC

A

release perforin into target cell –> pokes holes

release granzyem into target cell –> induces apoptosis

21
Q

IL-2

A

activates NK cells to kill tumor cells

22
Q

IL-12

A

stimulates NK cells to produce IFN gamma, which activates macrophages

23
Q

innate lymphoid cells

A

ILC1, ILC2, and ILC3

important in early responses to viruses, parasitic worms, and bacteria

24
Q

C3 convertase

A

cleaves C3 into C3a and C3b
C3a = chemokine
C3b = opsonin

25
Q

C5 convertase

A

cleaves C5 into C5a and C5b
C5a = chemokine
C5b = opsonin, forms MAC with C6-9

26
Q

most potent component of complement system

A

C5a

27
Q

complement component that is central to all three pathways

A

C3

28
Q

most concentrated complement component in serum

A

C3

29
Q

antibody that activates complement best

A

IgM is most efficient

IgG is second most efficient

30
Q

why is C3 not a stable molecule

A

reactive thioester bond allows spontaneous activation of alternative complement pathway

31
Q

chronic granulomatous disease

A

deficiency in expression/function of NADPH oxidase leads to inability to generate superoxide –> defect in killing intracellular bacteria –> increased susceptibility to bacterial infection

Microbiology/Immunology (30 decks)

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