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IAHI Block 3 > Host Defenses > Flashcards

Host Defenses Flashcards

1
Q

Innate Immune Response

A

Cytokine Response

NK Response

Complement

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2
Q

Adaptive Immune Response

A

Cytokine Response

T Cell Response

B cell Response (antibodies)

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3
Q

Innate Immunity after virus infection

A
  1. Recognition of patterns by PRRs
  2. Type I IFN secretion
  3. Secretion of other solule mediators:
    1. Cytokines - IL-1, TNFα, IFNγ, chemokines etc
  4. Complement
  5. NK cells
    1. Direct killing of virus infected cells
    2. Huge source of IFNγ production
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4
Q

Adaptive Immunity after virus infection

A
  1. Cytokines
  2. Cytotoxic T cells
    1. Granule exocytosis
    2. Fas L induced apoptosis
  3. B-cells and antibodies
    1. Neutralization
    2. Opsonization
    3. Phagocytosis
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5
Q

NK acitivity is 20-100x better when _____ and/or _____ or present

A

IFNs; IL-12

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6
Q

Interferon α use in virus infections

A
  • Used in the treatment of chronic Hepatitis C
  • Also used in the treatment of melanoma, hairy cell leukemia, chronic myelogenous leukemia, Kaposi’s sacroma
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7
Q

Inteferon ß used in treatment of ________ ________

A

Multiple Sclerosis

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8
Q

Why don’t we generally use Interferon γ

A

Side Effects:

  • Flu like symptoms following each injection
  • Problems with thinking and concentration
  • Reduce blood counts
  • These symptoms occur in up to half of all patients
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9
Q

The first response to virus infection: Type I Interferons (IFN- α/ß)

A
  • Viral products (dsRNA, ssDNA, unmethylated DNS)
  • Sensed by PRRs (TLRs)
  • Cascade of signaling through adaptors, kinases
  • Activates Transcription factors (IRFs - Interferon response factors bind to ISRE - Inteferon Stimulated Response Element)
  • Synthesis and secretion of IFN- α/ß (Induction of ANTIVIRAL STATE in nearby cells)
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10
Q

Signaling pathway used by Type I inteferons

A

Jak/STAT pathway

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11
Q

Type I IFNs activate ___ and ____ __________ ______

A

PKR; 2’-5’ Oligoadenylate Synthase

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12
Q

PKR (Protein Kinase R)

A
  • Binds to dsRNA and becomes autophosphorylated - it is a PRR
  • It then phosphorylates eIF-2α
  • eIF-2α delivers Met tRNA to the 40s ribosome to initiate polypeptide synthesis
  • When eIF-2 α is phosphorylated, translation is prevented
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13
Q

OAS (2’-5’ Oligoadenylate Synthetase is also induced by IFN)

A
  • Binds to and is activated by dsRNA
  • Catalyzes synthesis of oligo adenylate from ATP, through a 2’-5’ linkage
  • Oligo AAAA activates RNAse L - an endoribonuclease
  • Binding of RNAseL to oligo AAA induces dimeration (activation) of RNAse L, which degrades mRNA

End Result: mRNA degradation - shutdown of protein synthesis

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14
Q

IFN-α/ß induce the Anti-Viral State which consists of:

A

Increased:

  • MHC class I expression
  • PKR expression
  • 2’-5’ snthase expression
  • 2’-5’ oligo A (A-A)
  • Viral mRNA degradation
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15
Q

Pro Inflammatory Cytokines

A
  • TNF
    • A pyrogen - can induce fever
    • Produced by activated macrophages, CD4 T cells, and NK cells
  • IL-1ß
    • A pyrogen
    • Major pro-inflammatory cytokine
    • Produced and secreted by activated macrophages
  • IL-6
    • Major pro-inflammtory cytokine
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16
Q

NK cells kill targets after assessing the balance between…

A
  • Inhibitory signals from class I molecules
  • Activating signals from NK activating ligands
17
Q

Infected cells are often induced to undergo _______

A

apoptosis

18
Q

Two types of “programmed cell death”

A
  • From within (a protective “selfless” infected cell response)
  • From without (Fas or by TNF-α on cytotoxic T cells, NK cells)
19
Q

Cellular mechanisms of Apoptosis

A
  • Cytochrome C released from mitochondria by p53 interaction with Bax/Bak pores
  • Cytochrome C induces production of capsase-9 which becomes capsase-3
  • Causes cell death
  • TNF-R can also induce production of capsase-3
20
Q

How do viruses prevent IFN signaling extracellularly

A

Viruses encode proteins to prevent IFN binding to receptors

This protein binds to type 1 interferons preventing them from binding the actual receptors (same for IFN-γ)

21
Q

How do viruses prevent IFN signaling from within:

A
  • Viruses can encode their own structured RNA to bind to PKR and inhibits activation by dsRNA
  • Herpesvirus encode a protein that recruits a cellular phosphatase that cleaves the phosphate from eIf-2α
  • Poxviruses encode dsRNA binding proteins that sequester the dsRNA and prevent PKR activation
  • Poxviruses also encode eIF2α decoy that binds to PKR and prevents it from phosphorylating eIF2α
22
Q

Fever

A

Considered a component of host defense that enhances inflammatory and immune response - fever inducing candidates = IL-1/IL-6/TNF-α

23
Q

Poxvirus recominants lacking the _____ _____ _____ have been generated - when mice are infected with these viruses…they develop fevers

A

IL-1ß binding protein

24
Q

What prevents complements from destroying normal cells

A

Cells encode “Control” proteins on their surface that block complement activation. Bacterial surfaces lack these complement control proteins so complement can activate antibody-independent virolysis

25
Q

How do viruses avoid complement MAC complex

A

Can encode homologs of complement control proteins that prevent assembly of MAC complex

Can encapsidate viral or host complement control proteins in their membranes to evade complement-mediated lysis

26
Q

How do viruses avoid T-cell response (6)

A

Viruses strategize to affect the surface expression of MHC and NK ligands

  1. Degrade TAP transporter
  2. Block peptide transport into ER by blocking TAP transporter
  3. Degrade class I MHC molecules
  4. Retain class I MHC molecules in ER/Golgi
  5. Divert class I MHC to lysosomes, where it is degraded
  6. Downregulate transcription of components of the MHC molecule
27
Q

To evade NK cell killing, viruses can:

A
  • Modulate the removal of MHC-I from the surface of infected cells, removing some HLA-A and -B but leaving HLA-C on the surface
  • Encode decoy MHC-I-like molecules that interact with inhibitory NK receptors
  • Prevent activating NK cell receptor ligands from arriving at the cell surface by retaining them in the ER, or rerouting them to lysosomes
28
Q

Viruses induce the downregulation of other molecules in the immunological synapse:

A
  • Adhesion molecules (ICAM-I)
  • Costimulatory Molecules (CD80/CD86/B7)
29
Q

Viral mechanisms to prevent apoptosis

A
  1. Virus-encoded soluble TNF receptors
  2. VIral inhibitors of capsases that block various proteolytic steps of capsase activation and target protein cleavage
  3. Virus-encoded homologs of “anti-apoptotic” proteins such as Bcl-2
  4. Virus-encoded inhibitors of p53, a major inducer of “apoptosis from within”

IAHI Block 3 (17 decks)

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