2- Innate Immunity Flashcards

1
Q

How does an exotoxin damage host tissues?

A

binds to a specific cell surface receptor

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2
Q

How does an endotoxin damage host tissues?

A

It stimulates phagocytes to secrete cytokines and cause local or systemic symptoms

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3
Q

What is the direct cytopathic effect?

A

Intracellular destrction by an an intracellular bacteria or virus.

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4
Q

What is the complement system?

A

The first defense against pathogens using proteins that coat and kill the bacteria.

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5
Q

What is the most important protein for the complement system?

A

C3

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6
Q

How is the alternative pathway activated?

A

Triggered by microbial surface membranes or other innate immunity components.

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7
Q

How is the lectin pathway activated?

A

Mannose-binding lectin binding to the pathogen surface.

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8
Q

How is the innate classical pathway activated?

A

CRP

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9
Q

How is the adaptive classical pathway activated?

A

By the binding of antibodies to the bacterial surfaces.

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10
Q

Cleavage of C3 peptide yields what 2 important complement proteins?

A

C3a and C3b

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11
Q

What is the function of C3a?

A

It’s an anaphylatoxin

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12
Q

What is the function of C3b?

A

It’s an opsonin

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13
Q

What is the function of C4b?

A

It’s an opsonin

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14
Q

What is the function of C5a?

A

It’s both an anaphylatoxin and chemotractant

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15
Q

What is the cause of hereditary angioedema?

A

A lack of C1 inhibitor. This allows the complement process to continuously run and causes edema in various organs and tissues.

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16
Q

What is the end result of the complement system?

A

Membrane Attack Complex (MAC)

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17
Q

What is the C# convertase of the alternative complement pathway?

A

C3bBb

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18
Q

Why is C3bBb the amplification step of the alternative pathway?

A

Since it’s the C3 convertase and bound to the surface of the pathogen, lots of C3b is made and covers the pathogen for opsonization.

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19
Q

What is the function of CR1?

A

Since it’s on the macrophage, it binds to C3b on the pathogen and eats it.

20
Q

What is the function of CR3 and CR4?

A

Same as CR1. On the macrophage, binds to C3b and allows the macrophage to feast.

21
Q

What proteins compose the MAC?

A

C5-9

22
Q

What infections might occur if there is a deficiency in any C5-9 proteins?

A

Neisseria infections

23
Q

What does the MAC do?

A

Make holes in the membranes of the bacteria.

24
Q

How do C3a and C5a act as anaphylatoxins?

A

They induce smooth muscle contraction and degrtanulation of basophils and mast cells.

25
Q

What is the general function of defensins?

A

They are + charged molecules that attract the - charged proteins of the pathogens, penetrate the membranes of the pathogens and destroy them.

26
Q

Where are α –defensins from?

A

Neutrophils and other cells of innate immunity like Paneth cells of the GI

27
Q

Where are β-defensins from?

A

Most epithelial surfaces- skin, respiratory, and urogenital tract.

28
Q

What is the process of macrophage activation and completion of phagocytosis?

A

Macrophage recognizes pathogen structures using various receptors –> M0 binds the pathogen –> internalize in a phagosome –> lysosome fuses with phagosome –> everything in the phagosome is destroyed

29
Q

What are toll-like receptors (TLR’s)?

A

They are signalling receptors on cells that allows the body to detect pathogens based on pathogen structures. The “watchdogs” of the body.

30
Q

What are the function of IL-1β from macrophages?

A

They locally activate the lymphocytes and tissue destruction.

31
Q

What are the functions of TNF- α from macrophages?

A

Locally they increase vascular permability, systemically they induce fever.

32
Q

What are the functions of IL-6 from macrophages?

A

Induce fever systemically

33
Q

What is the function of CXCL8 (IL-8) from macrophages?

A

It’s a local chemotactic factor for PMN’s

34
Q

What are the functions of IL-12 from macrophages?

A

Locally they activate NK cells to secrete IFN-γ

35
Q

How does LSP activation of macrophages lead to septic shock?

A

LPS causes a widespread production of TNF- α, which dilates blood vessels and causes a massive leakage of fluids into tissues throughout the body.

36
Q

What are the 1st type of WBC to a site of infection?

A

Neutrophils

37
Q

How are neutrophils attracted to a site of infection?

A

CXCL8 from macrophages and C5a from the complement

38
Q

What are the 4 steps of extravasation of neutrophils into tissues

A
  1. Rolling adhesion (selectins on neutrophil bind to vessel wall), 2. Tight binding (using integrin and CXCL8), 3. Diapedesis (sqeeze through the wall), 4. Migration (using CXCL8 gradient to infection)
39
Q

What is the cause of the respiratory burst?

A

Neutrophils, when they eat, increase O2 consumption, subsequently making superoxide radicals and H2O2

40
Q

What are the 3 proinflammatory cytokines?

A

IL-1, IL-6 and TNF-α

41
Q

What occurs during the acute phase response?

A

Acute phase proteins like mannose-binding lectin and CRP are made to enhance fixation of the complement on pathogens.

42
Q

What are the 2 functions of CRP?

A

Act as an opsonin and it triggers the classical complement pathway

43
Q

What are the 2 main functions of IFNα and IFNβ?

A
  1. to interfere with viral replication and 2. activate NK cells to kill virus infected cells.
44
Q

What are the 2 main functions of NK cells?

A
  1. to kill the infected cells using cytotoxic granules and 2. to release IFN-γ which recruits macrophages to the infection.
45
Q

What receptor on NK cells bind to the MIC-A and B of infected cells?

A

NKG2D