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SFM Exam 1 > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

What would occur in the absence of innate immunity?

A

The invading pathogens would grow uncontrollably and kill the host

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2
Q

What would happen in the absence of adaptive immunity?

A

Infections are initially controlled by innate immunity however the invading pathogen can not be eliminated completely

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3
Q

Which cells are the main defense against extracellular infection (bacteria)?

A

Abs and PMNs

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4
Q

Which cells are the main defense against intracellular infection (viruses)?

A

CTLS, NK cells, macrophages

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5
Q

Neutrophil function

A

Early phagocytosis and killing of microbes

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6
Q

NK cell function

A

Lysis of infected cells, activation of macrophages

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7
Q

Function of C-reactive protein

A

Opsonization of microbes and activation of complement

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8
Q

Function of TNF, IL-1 and chemokines

A

Inflammation

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9
Q

Function of IFN-alpha and beta

A

Resistance to viral infection
Local effect: inhibition of viral gene replication
Up regulate expression of MHC class I molecules

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10
Q

IFN-gamma function

A

Macrophage activation

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11
Q

IL-12 function

A

Potent inducer of IFN-gamma production by NK cells and T cells

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12
Q

IL-15 function

A

Proliferation of NK cells

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13
Q

IL-10 and TGF-beta function

A

Control of inflammation

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14
Q

In most cases innate immune response to pathogens

A

Prevents, controls or eliminates infection without engagement of adaptive immunity

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15
Q

Innate immunity also functions to eliminate host damaged cells and initiate the process of tissue repair that involves

A

Recognition of stressed, damaged and/or dead host cells, phagocytosis and clearance of cellular debris, and stimulation and control tissue remodeling

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16
Q

IFN-gamma/IL-12 amplification loop

A

Macrophages secrete IL-12 which stimulates the NK cells to produce IFN-gamma
IFN-gamma activates phagocytosis and killing of microbes by macrophages

17
Q

Macrophages treated with IFN-gamma exhibit a classical activation profile that is characterized by

A

Increased synthesis of pro-inflammatory cytokines, increased production of ROS, synthesis of inductive NOS, up-regulation of lysosomal enzymes and enhances Ag presenting properties

18
Q

Killing of a host cell by NK cells will always occur if either

A

MICA/MICB expression is increased or class I MHC expression is decreased

19
Q

What systemic effects are produced by IL-1, TNF-alpha and IL-6?

A

Fever (potency: IL-1>TNF>IL-6)
Induction of acute phase proteins (IL-6>IL-1>TNF-alpha)
Arthralgia/myalgia (TNF-alpha)

20
Q

Virus Ag-activated B cells produce low affinity/high avidity anti-viral IgM but B cells educated by Th2 cells differentiate and switch production of

A

Low affinity/high avidity anti-viral IgM to high affinity anti-viral IgG or IgA of exactly the same specificity

21
Q

What are the local affects of TNF and IL-1?

A

Increased adhesion and permeability of blood vessels as well as activation of leukocytes

22
Q

What are the systemic pathological effects of TNF?

A

Low CO, thrombus and increased permeability of blood vessels, insulin resistance effecting multiple tissues

23
Q

When infected with coronavirus what cytokines are released by macrophages?

A

TNF-alpha, IL-1 beta, IL-6 and IL-18 (liver damage)

24
Q

Which cytokines are involved in septic shock/sepsis associated tissue injury?

A

TNF-alpha, IL-1 (involved in regulation of fever)and IL-6 (regulates synthesis of acute phase proteins)
Also involved in leukocyte activation and SIRS

25
Q

Which cytokines are well known anti-inflammatory cytokines?

A

IL-10, soluble IL-1 receptor antagonist, IL-4 and TGF-beta

Partially responsible for CARS, involved in leukocyte deactivation and sepsis associated immunosuppression

26
Q

Which patient population usually die due to the overwhelming SIRS?

A

Young and previously healthy patients

Early deaths due to overwhelming hyper-inflammatory response

27
Q

Which pt population usually dies due to the overwhelming CARS?

A

Elderly chronic pt

Late deaths due to persistent immunosuppression

28
Q

Characteristics of C reactive protein (CRP)

A

Located in serum and interstitial fluid
Binds to microbial polysaccharides and lipopolysaccharides (LPS)
Binding of CRP to these bacterial substrates activates the classical complement pathway

29
Q

Gram positive bacteria are recognized by which TLRs?

A

TLR2/6

30
Q

Gram negative bacteria are recognized by which TLRs?

A

TLR4

31
Q

DCs bias differentiation of T cells towards either

A

T helper type 1 (Th1) cells which control immune responses against intracellular pathogens or
Th2 cells which control immune responses against extracellular pathogens

32
Q

Describe IgM affinity and avidity

A

IgM has low affinity of Ag binding that is compensated by the existence of 10 Ag binding sites on the molecule
IgM exhibits high avidity binding when multiple Ag binding sites are engaged in interaction with bacteria

33
Q

Which Ab is a very potent complement activator that generates C3b?

A

IgM

34
Q

What is opsonization?

A

An immune response process which uses opsonins (ex. C3b and Abs) to tag foreign pathogens for elimination by phagocytes

35
Q

What would occur without an opsonin such as an Ab or C3b?

A

The negatively charged walls of the pathogen and phagocyte would repel each other and the pathogen could then avoid destruction and continue to replicate inside the human body

36
Q

What is an important bridge between innate and adaptive immunity?

A

Pathogen recognition through PRRs
Ex. PRRs such as TLRs cause activation and maturation of APCs and then Ag processed by APCs are presented to naive T cells

37
Q

IL-12 controls the development of

A

Th1 cells specific for intracellular pathogens

38
Q

IL-4 controls the development of

A

Th2 cells specific for extracellular pathogens

SFM Exam 1 (8 decks)

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