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SFM Exam 1 > 4: Innate Immunity > Flashcards

4: Innate Immunity Flashcards

1
Q

Four intracellular pathogens + four extracellular pathogens

A

Intracellular: bacteria, Protozoa, viruses, mycobacterium

Extracellular: bacteria, Protozoa, parasites, fungi

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2
Q

Four major players in intracellular infections

A

CTLs, NK cells, T cells, macrophages

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3
Q

Three major players in extracellular infections

A

Neutrophils, Abs, complement

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4
Q

What is an important bridge between innate and adaptive immunity?

A

PRRs

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5
Q

What can PRRs do?

A

Cause activation/maturation of APCs

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6
Q

What cytokines direct development of Th1 and Th2?

A

Th1: IL-12
Th2: IL-4

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7
Q

Th1 vs Th2: intracellular vs extracellular pathogens?

A

Th1: intracellular
Th2: extracellular

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8
Q

Major cytokine that mediates innate immunity

A

IFN type 1

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9
Q

What cytokine is released by virally infected cells?

A

IFN type I (a/B)

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10
Q

What do viruses release from host cells to activate macrophages and DCs?

A

PAMPs and DAMPs

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11
Q

Where do virally infected cells present their viral peptides?

A

MHC Class I

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12
Q

Five cytokines from macrophages and their functions

A

IL-8: recruit neutrophils
MCP-1: recruit monocytes
IL-1, TNF-a, IL-6: acute phase response

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13
Q

What is the acute phase response? (Three cytokines, three effects)

A

Formed by IL-1, TNF-a, and IL-6 -> causes fever, APP induction, and arthralgia/myalgia

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14
Q

Potency of cytokines causing fever

A
  1. IL-1
  2. TNF-a
  3. IL-6
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15
Q

Potency of cytokines causing APP induction

A
  1. IL-6
  2. IL-1
  3. TNF-a
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16
Q

What one cytokine causes arthralgia/myalgia?

A

TNF-a

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17
Q

How do DCs bias CD4 differentiation

A

Based on whether DC has a viral or bacterial Ag

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18
Q

Two cytokines by Th1 cells and their functions

A

IL-1: in LN, proliferation of CTLs

IFN-y: stimulate macrophages

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19
Q

Which two cell types must work with macrophages bc they dont kill viral particles, just kill host cells

A

NK cells, CTLs

20
Q

What two cytokines increase CTL resistance to apoptosis?

A

IFN-y, IL-2

21
Q

First Ig produced by B cells + its affinity and avidity

A

IgM - low affinity, high avidity

22
Q

Why is IgM high avidity?

A

10 binding sites

23
Q

How do B cells learn how to isotype switch to IgG and IgA?

A

By interaction with Th2 cells

24
Q

When Abs act as opsonin, what two things do they attach to?

A
  1. Epitope on Ag

2. Fc portion binds phagocyte receptor

25
Q

What two stress-associated molecules are presented on infected cells acting as killing signals for NK cells?

A

MICA, MICB

26
Q

Two receptor types on NK cells and what they recognize on infected cells

A
  1. KARS: recognize MICA, MICB

2. KIRS: recognize class I MHC

27
Q

KAR vs KIR activation in NK cells

A

KAR activation -> activation of protein tyrosine kinases in NK cell

KIR activation -> activation of protein tyrosine phosphatases in NK cell

28
Q

How are NK cells activated by microbes?

A

They are not

29
Q

Three steps in NK cell killing

A
  1. Perforins -> make a hole
  2. Granzymes -> enter hole and digest enzymes
  3. Enemy cell undergoes apoptosis
30
Q

Macrophage/NK amplification loop

A
  1. Macrophages make IL-12 -> stimulate NK cells to produce IFN-y
  2. IFN-y activates macrophages to phagocytose
31
Q

What type of activation occurs when macrophages are activated with IFN-y

A

Classical M activation

32
Q

Two principle pathogenic mechanisms of bacteria

A
  1. Inflammation/tissue destruction

2. Bacterial toxin

33
Q

Bacterial endotoxins vs exotoxins

A

Endotoxins: in bacterial cell walls, not released by living bacteria
Exotoxins: constantly secreted by bacteria

34
Q

Example of an endotoxin

A

LP: in gram negative bacteria

35
Q

Three examples of bacterial exotoxins

A

Diphtheria toxin, cholera toxin, tetanus toxin

36
Q

What complement pathway can CRP activate?

A

Classical pathway

37
Q

Major job of C3b

A

Opsonize bacteria -> bind CR1 on macrophage/neutrophil surface to recruit phagocytes to engulf bacteria

38
Q

How does opsonization bring bacteria and phagocyte together?

A

It allows two negatively charged cell walls to come together

39
Q

Name for C3a and C5a

A

Anaphylatoxins

40
Q

Three functions of anaphylatoxins

A
  1. Activate mast cells
  2. Mediate leukocyte chemotaxis
  3. Attract neutrophils to infection
41
Q

What do mast cells release and what does this do?

A

Histamine and proteases -> enhanced blood flow -> edema, itchiness, irritation

42
Q

Macrophage function on endothelial cells

A

Increases CAMs, especially P/E selectins

43
Q

What TLRs recognize gram positive vs gram negative bacteria

A

Gram positive: TLR2, TLR6

Gram negative: TLR4

44
Q

What does local inflammation around an LN cause

A

Upregulation of CAMs on HEVs -> T and B cells enter en masse

45
Q

Four major players in helminths infections

A
  1. Eosinophils
  2. Basophils
  3. Mast cells
  4. IgE
46
Q

Which Th cell is important in fungal infections, and which facilitates the fungus?

A

Th1 fights fungus, Th2 helps fungus

SFM Exam 1 (17 decks)

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