Innate Immunity Flashcards

1
Q

What is rule one?

A

most bacterial die inside phagocyte

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2
Q

endotoxins

A

recognized by our immune cells to give us a response, one way to recognize bacteria and pick them up, not necessarily toxic, membrane component of cell wall, could cause our body to produce toxic molecules

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3
Q

Lipopolysaccharide (LPS)

A

gram negative bacteria, heat stable, will go through filters, measured using Limulus Amebocyte Lysate assay, negative reagents are called pyrogen free (does not cause fever in rabbits), can be destroyed by baking glassware at high temperature

toxic component of some gram negative bacteria

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4
Q

gram negative sepsis

A

caused by body’s response to endotoxins, can be the result of a major trauma, car accident, or contaminated IV solution. results in Disseminated Intravascular Coagulation (DIC), Acute Respiratory Distress Syndrome (ARDS), hypovolemic shock with decreased blood pressure

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5
Q

Limulus Amebocyte Lysate assay

A

used to measure LPS

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6
Q

IL-6

A

secreted by macrophages, fever, induces acute phase product production by hepatocytes

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7
Q

TNF alpha

A

activates vascular endothelium and increases vascular permeability, which leads to increased entry of complement and cells to tissues and increased fluid drainage to lymph nodes

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8
Q

IL-1 beta

A

activates vascular endothelium, activates lymphocytes, local tissue destruction, increase access of effector cells

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9
Q

Toll Like Receptor (TLR)

A

binds bacterial LPS, assisted by CD14

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10
Q

bacterial superantigen

A

made by some bacteria, crosses constant region of MHC and TCR, binding results in large amount of IL-1 and TNF, results in symptoms that look like gram negative sepsis

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11
Q

Complement

A

one of the critical ways we recognize foreign particles when they come into our body. easily killed by heat, does not increase during immunization (unlike antibodies).

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12
Q

alternative pathway (overview)

A

pathogen surface creates local environment conducive to complement activation

innate pathway that leads to pathogen surface recognition that leads to recruitment of inflammatory cells, opsonization of pathogens, facilitating uptake and killing by phagocytes, perforation of pathogen cell membranes

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13
Q

classical pathway (overview)

A

C reactive protein or antibody binds to specific antigen on pathogen surface

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14
Q

classical pathway steps

A

C1q/C1r/C1s binds to single IgM (or 2 IgG) and cleaves C4 leaving C4b bound to the pathogen surface. C1 complex cleaves C2 leaving C2a bound to C4b. C4b2a cleaves C3 to leave C3b bound to pathogen surface.

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15
Q

alternative pathway steps

A

C3 spontaneously lyses with B to create C3bBb on pathogen surface. C3bBb lyses C3 to leave C3b bound on pathogen surface

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16
Q

Two types of C3 convertase

A

C4b2a from classical, C3bBb from alternative pathway.

17
Q

Properdin

A

stabilizes C3 convertase C3bBb on a pathogen surface

18
Q

factor H and factor I

A

inactivates C3b to leave iC3b on pathogen surface. iC3b can still be target for activation

19
Q

DAF and MCP

A

disrupts C3 convertase C3bBb on human cell surface. Inhibits production of C3bBb complex.

20
Q

Deposition of C3b leads to

A

binding to complement receptors that allow opsonization and clearance of immune complexes

21
Q

immune complexes

A

cleared by complement system with the help of RBC

22
Q

C5a

A

critically important chemotactic factor, causes leukocytes to come to bacteria, starts lytic pathway

23
Q

lytic pathway

A

results in C9 creating a complex on the pathogen that punches pore in the membrane

24
Q

C1, C2, C4 (classical pathway) deficiency

A

cannot clear antibody complexes

25
Q

C3 (opsonization pathway) deficiency

A

susceptible to serious bacterial infections

26
Q

C5-C9 (lytic pathway) deficiency

A

susceptibility only to Neisseria

27
Q

what molecules made by our bodies can mediate septic shock

A

TNF alpha and IL-1

28
Q

membrane attack complex

A

formed by components C5-C9, lyses target cell

29
Q

CR1

A

receptor on phagocytes that bind C3b