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
What two stress-associated molecules are presented on infected cells acting as killing signals for NK cells?
MICA, MICB
26
Two receptor types on NK cells and what they recognize on infected cells
1. KARS: recognize MICA, MICB | 2. KIRS: recognize class I MHC
27
KAR vs KIR activation in NK cells
KAR activation -> activation of protein tyrosine kinases in NK cell KIR activation -> activation of protein tyrosine phosphatases in NK cell
28
How are NK cells activated by microbes?
They are not
29
Three steps in NK cell killing
1. Perforins -> make a hole 2. Granzymes -> enter hole and digest enzymes 3. Enemy cell undergoes apoptosis
30
Macrophage/NK amplification loop
1. Macrophages make IL-12 -> stimulate NK cells to produce IFN-y 2. IFN-y activates macrophages to phagocytose
31
What type of activation occurs when macrophages are activated with IFN-y
Classical M activation
32
Two principle pathogenic mechanisms of bacteria
1. Inflammation/tissue destruction | 2. Bacterial toxin
33
Bacterial endotoxins vs exotoxins
Endotoxins: in bacterial cell walls, not released by living bacteria Exotoxins: constantly secreted by bacteria
34
Example of an endotoxin
LP: in gram negative bacteria
35
Three examples of bacterial exotoxins
Diphtheria toxin, cholera toxin, tetanus toxin
36
What complement pathway can CRP activate?
Classical pathway
37
Major job of C3b
Opsonize bacteria -> bind CR1 on macrophage/neutrophil surface to recruit phagocytes to engulf bacteria
38
How does opsonization bring bacteria and phagocyte together?
It allows two negatively charged cell walls to come together
39
Name for C3a and C5a
Anaphylatoxins
40
Three functions of anaphylatoxins
1. Activate mast cells 2. Mediate leukocyte chemotaxis 3. Attract neutrophils to infection
41
What do mast cells release and what does this do?
Histamine and proteases -> enhanced blood flow -> edema, itchiness, irritation
42
Macrophage function on endothelial cells
Increases CAMs, especially P/E selectins
43
What TLRs recognize gram positive vs gram negative bacteria
Gram positive: TLR2, TLR6 | Gram negative: TLR4
44
What does local inflammation around an LN cause
Upregulation of CAMs on HEVs -> T and B cells enter en masse
45
Four major players in helminths infections
1. Eosinophils 2. Basophils 3. Mast cells 4. IgE
46
Which Th cell is important in fungal infections, and which facilitates the fungus?
Th1 fights fungus, Th2 helps fungus