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Immunology > Innate Immunity > Flashcards

Flashcards in Innate Immunity Deck (29):
1

What is rule one?

most bacterial die inside phagocyte

2

endotoxins

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

3

Lipopolysaccharide (LPS)

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

4

gram negative sepsis

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

5

Limulus Amebocyte Lysate assay

used to measure LPS

6

IL-6

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

7

TNF alpha

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

8

IL-1 beta

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

9

Toll Like Receptor (TLR)

binds bacterial LPS, assisted by CD14

10

bacterial superantigen

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

11

Complement

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).

12

alternative pathway (overview)

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

13

classical pathway (overview)

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

14

classical pathway steps

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.

15

alternative pathway steps

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

16

Two types of C3 convertase

C4b2a from classical, C3bBb from alternative pathway.

17

Properdin

stabilizes C3 convertase C3bBb on a pathogen surface

18

factor H and factor I

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

19

DAF and MCP

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

20

Deposition of C3b leads to

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

21

immune complexes

cleared by complement system with the help of RBC

22

C5a

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

23

lytic pathway

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

24

C1, C2, C4 (classical pathway) deficiency

cannot clear antibody complexes

25

C3 (opsonization pathway) deficiency

susceptible to serious bacterial infections

26

C5-C9 (lytic pathway) deficiency

susceptibility only to Neisseria

27

what molecules made by our bodies can mediate septic shock

TNF alpha and IL-1

28

membrane attack complex

formed by components C5-C9, lyses target cell

29

CR1

receptor on phagocytes that bind C3b