Innate Immunity Flashcards

1
Q

Endotoxins

A

Heat-stable (pyrogen) cell-associated toxin
NOT directly TOXIN
Induces body to produce toxic molecules

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2
Q

LPS

A

Endotoxin on gram - bacteria

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3
Q

Pathology of LPS

A

LPS responsible for many of the body’s responses to gram negative bacteria

  • profound inflammatory response
  • infiltration of neutrophils and MOs
  • increases permeability
  • swelling
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4
Q

Septic shock

A

Endotoxin shock - associated w/ gram - infection

  • lethal
  • can lead to DIC, necrosis, ARDS
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5
Q

How to avoid Endotoxins

A

Test for pyrogen using LAL

-if dev DIC - there is LPS present

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6
Q

What toxic about LPS?

A

Proteins produced by LPS-stimulated MOs are the endogenous mediator (inflammatory cytokines)

  • *IL-1
  • *TNF-Alpha
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7
Q

TNF-Alpha

A

Important cytotoxic molecule produced by MO and is an important immunoregulator molecule

  • Has overlapping function w/ IL1
  • -stimulating B and T cells
  • -inducing fever
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8
Q

IL-1

A

Cytokine secreted by activated and stimulated MOS
_produced as a pro-cytokine (must be cleaved prior to release)
_cleavage often by caspase 1 activated by inflammation sensitive complex (inflammasome)

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9
Q

Super Agtigenic Toxins

A

TSST-1 - endotoxin causing toxic show syndrom
-In response to the binding of toxin
__both T cells and APC produce many cytokines
–>TNF-alpha and IL1

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10
Q

Complement System

A
  • Much more than lead to cell lysis
  • Imp inflammatory mediators
  • Role in opsonization
  • Imp in clearing immune complexes
  • Terminal complement imp in killing Neisseria
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11
Q

Complement

A

Is the collective term for a complex of sequentially interacting serum proteins

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12
Q

What occurs as a result of complement activation cascade?

A
Cell lysis
Increased phagocytosis
Increased vascular permeability
Enhance leukocyte chemotaxis
Functional stimulation of MOs
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13
Q

What are the two PWs for complement?

A

Classical PW
Alternative PW
**both lead to cleavage of C3 –>C3a and C3b
C3b attaches to surface of pathogen

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14
Q

Classical PW

A
  • Initiation by IgM or IgG binding to Ag on a pathogen surface
  • C1 binds single molecule of IgM (pentamer) or 2 or more IgG
  • Activated C1s cleave C4 and C2
  • C2a binds to surface C4b - forming C3b convertase (C4b2a)
  • binds to C3b and cleaves it
  • C3b binds covalently to microbial surface
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15
Q

Alternative PW

A

Formation and action of the soluable C3 convertase iC3Bb that initiates this PW

  • -formation and action of the C3 convertase (C3bBb) at a pathogen surface
  • -C3 continuously cleaved and C3b put on pathogen surface
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16
Q

Inactivation of C3b

A
  • Inactivation of C3b by factor H and factor I to give fragments iC3b
  • DAF and MCP disrupt C3 convertase C3bBb on a human cell surface
17
Q

How are bacteria recognized by INNATE immune response?

A

By Endotoxins and Complement

–w/o them you DON’T get ADAPTIVE immune response

18
Q

What do phagocytes do when react with bacteria?

A

Release cytokines

-too many is bad

19
Q

Release of cytokines

A

Locally - its good

Systemically - its bad–> they become part of pathology

20
Q

What are the receptors that interact with LPS ?

A

Recognized by the complex TLR4, MD2, and CD14 (part of LPS receptor - TLR4)

  • leads to engulfment and digestion of bacteria
  • lead to transcription of inflammatory cytokines
21
Q

TLR’s

A

Diff TLRs are recognize diff things and respond differently

22
Q

Why is inflammasome important?

A

Important for IL1 production

23
Q

Both complement PWs lead to C3b on pathogen surface in order to…?

A

Amplify C3b

24
Q

What does C3b lead to?

A

Binding to complement receptors

  • ->Opsonization
  • ->Clearance of immune complexes
25
Q

What occurs when IgG binds to SOLUABLE multivalent Ag?

A
  • C1 binds to soluable immmune complex (Ag:Ab) and initiates complement rxn
  • Immune complex coated with covalently bound C3b
  • C3b binds to receptor on erythrocyte surface
  • Erythrocyte takes them to spleen/liver where they are removed by phagocytic cells
  • *classical PW clears complex
26
Q

What imp role does classical PW play?

A

Clear immune complexes out of blood

27
Q

C5 Convertase

A

Activated by both PWs

**IMP Chemotactic Factor (attracts MO, nuetrophills, etc)

28
Q

Lytic PW

A

Contains C5-C9

  • Components binds to surface of pathogen or RBC coated w/ Ab
  • Forms pores
  • Cell dies
29
Q

What are the biological active peptides?

A

C3a and C5a = anaphylatoxins

  • make cell leaky
  • draw monocytes/nuetrophils to site
30
Q

What are ANAPHYLATOXINS?

A

Make blood vessels leaky around where complement being fixed

  • causes them to be more fluid
  • complement, Ab, and more cells come to site of infection
31
Q

Inhibitors of complement system?

A
  • C1INH inhibits C1
  • C4BP binds to C4 in classical PW and makes it a target for factor I inhibition
  • Factor H binds C3b and makes it target for factor I - inactivates C3b –> iC3b
  • DAF and MCP disrupt C3 convertase C3bBb
32
Q

What is C59?

A

Binds to C5b678 complex and prevents recruitment of C9 to form pore

33
Q

C1, C2, C4 deficiency causes?

A

Immune-complex disease

-cant clear immune complex from blood

34
Q

C3 deficiency causes?

A

Susceptible to capsulated bacteria

35
Q

C5-C9 deficiency causes?

A

Susceptible to Neisseria

36
Q

Factor D and Factor P deficiency causes?

A

Susceptible to capsulated bacteria and Neisseria but not immune-complex disease

37
Q

Factor I deficiency causes?

A

Susceptible to capsulated bacteria

38
Q

DAF or CD59 deficiency causes?

A

Auto-immune like conditions

39
Q

C1lNH deficiency causes?

A

HANE