Lecture 20 Flashcards

1
Q

What is the function of CRP and SAP?

A

Acute phase proteins (APPs) that bind to bacterial surfaces (phosphocholine), bind to globular heads of C1q and activate classical complement pathway

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2
Q

Which complement pathways are activated by lipopolysaccharides?

A

Alternative and classical

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3
Q

What do C3a and C5a do?

A

Bind to receptors on mast cells and activate them

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4
Q

What do activated mast cells do?

A

Degranulate, releasing large amounts of histamine and bradykinin that enhances blood flow; causes arteriolar vasodilation, venous constriction in some vascular beds, and increased capillary permeability; increased blood flow and local edema are perceived as itchiness and irritation

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5
Q

What is the first cell to release cytokines and chemokines?

A

Mast cells

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6
Q

What are the potent neutrophil chemoattractants?

A

C5a, C3a, IL-8/CXCL8

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7
Q

What do immature DCs do during an extracellular bacteria infection?

A

Engulf and internalize bacteria (Ags) via PRRs (TLRs)

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8
Q

What do activated DCs do during an extracellular bacteria infection?

A

Migrate to local LNs via lymphatics

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9
Q

What causes the swelling and local hyperemia in LNs?

A

Lymphocytes become trapped, activated, and proliferate in inflamed LNs

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10
Q

What is responsible for the homing of lymphocytes to LNs?

A

L-selectin on lymphocytes and PNaD (peripheral lymph node addressin) on HEVs

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11
Q

Infections caused by pathogenic extracellular bacteria have 2 principle mechanisms. What are they?

A
  1. Tissue damage is caused by inflammation at the site of infection
  2. Bacteria produce toxins which have diverse pathologic effects
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12
Q

Define endotoxins and exotoxins

A

Endotoxins: components of bacterial cell walls

Exotoxins: secreted by bacteria

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13
Q

What is the function of Th17 cells? What effect do genetic defects in Th17 development have?

A

Promote local inflammation and recruit neutrophils and monocytes at sites of bacterial infection; genetic defects result in increased susceptibility to bacterial and fungal infections, with formation of multiple skin abcesses

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14
Q

Define septic shock and septic shock syndrome?

A

Septic Shock: severe pathological consequence of disseminated bacterial infection (sepsis) by some gram-negative/positive bacteria

Septic Shock Syndrome: characterized by circulatory collapse and disseminated intravascular coagulation

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15
Q

What is the main function of IL-10?

A

Major suppressor of macrophage function

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16
Q

Explain bacterial superantigens?

A

Bind to class II MHC outside the peptide-binding groove and bind to the variable region of different TCR-beta chains, regardless of the peptide specificity; therefore, superantigens can activate a large number of T cells causing polyclonal T cell activation

17
Q

What is Kawasaki disease?

A

Acute, multi-system vasculitis of unknown etiology; evidence suggests that it is a superantigen mediated disease

18
Q

What is the endogenous pathway of antigen presentation?

A

Proteins from intracellular pathogens are degraded by the proteasome and the resulting peptides are shuttled into the ER by TAP proteins; these peptides are loaded onto MHC class I and then delivered to the cell surface

19
Q

What is the exogenous pathway of antigen presentation?

A

Extracellular pathogens are engulfed by phagosomes; inside the phagosome, the pathogen-derived peptides are loaded onto MHC class II molecules, which activate Th cells that stimulate the production of Abs

20
Q

What is responsible for the detection of beta-glucan?

A

Dectin-1

21
Q

What is the major receptor involved in the nonopsonic recognition of fungi?

A

Macrophage mannose receptor