Chapter 16 - Part 1 Flashcards Preview

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Flashcards in Chapter 16 - Part 1 Deck (59)
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1
Q

what does mast cell degranulation do? what is it perceived as?

A

enhance blood flow

itchiness and irritation

2
Q

what attracts neutrophils to infection sites?

A

C5a, IL-8, and bacterial products

3
Q

where are bacterial Ags processed and presented?

A

local LNs

4
Q

what are processed bacterial proteins presented to?

A

Class II MHC molecules for differentiation of naive T cells

5
Q

TRUE or FALSE:

Initially, IgM class Ab is produced, then affinity maturation, isotype switching, and finally clonal expansion.

A

FALSE

Isotype switching occurs LAST

6
Q

in the resolution of an infection, what removes bacterial debris?

A

local macrophages and neutrophils, or by Abs

7
Q

infections caused by pathogenic extracellular bacteria have what 2 mechanisms?

A
  1. inflammation causing tissue destruction

2. production of toxins with diverse pathological effects

8
Q

what are bacterial toxins subdivided into?

A

endotoxins - bacterial cell wall components

exotoxins - secreted by the bacteria

9
Q

what is a common endotoxin and what does it activate?

what can it lead to?

A

LPS activates macrophages, DCs and endothelial cells

leads to gram negative sepsis

10
Q

what are 3 common extotoxins which are cytotoxic? what are their methods of action?

A

diphtheria - shuts down protein synthesis
cholera - ion/water transport interference
tetanus - inhibits neuromuscular transmission

11
Q

what can exotoxins stimulate the production of?

A

cytokines that cause disease

12
Q

what are the main mechanisms of innate immunity to extracellular bacteria?

A

complement act.
phagocytosis
inflammation

13
Q

what activates the alternative complement system?

A

Peptidoglycans (gram +) and LPS (gram -) bacteria

14
Q

what does the MAC lyse?

A

bacteria (Neisseria)

15
Q

What are the 3 major effectors of the complement system?

A

anaphylatoxins (C4a/C3a/C5a)
opsonins (C3b)
MAC

16
Q

What are the 3 mechanisms of prevention of host bystander damage (regulation)?

A

Factor I cofactor activity
Decay-acceleration activity for C3
Inhibition of lysis

17
Q

what prevents C3b from forming active convertases?

A

Factor I
MCP
CR1
Factor H

18
Q

what prevents C4b from forming an active convertase?

A

Factor I
MCP
CR1
C4BP

19
Q

what proteins inhibit the classical pathway?

A

DAF
CR1
C4BP

20
Q

what proteins inhibit the alternative pathway?

A

DAF
CR1
Factor H

21
Q

What factors inhibit the MAC formation?

A

CD59
Vitronectin
S protein

22
Q

Neutrophils and macrophages use surface ______ to recognize extracellular bacteria?

What receptors do they use to recognize bacteria opsonized with Abs and complement proteins?

A

mannose and scavenger receptors

Fc and complement receptors

23
Q

what ingests and destroys bacteria?

A

recruited leukocytes

24
Q

what does TLR1 and 2 recognize?

A

lipoprotein

25
Q

What does TLR4 recognize?

what amplifies the detection?

A

LPS

CD14

26
Q

What does TLR5 recognize?

A

flagellin

27
Q

what does TLR9 recognize?

A

CpG DNA

28
Q

what is the most important activator of the inflammatory response?

what adaptor protein is required?

A

NF-KB

MyD88

29
Q

what detects intracellular pathogens?

A

NOD2 and NLRP3

30
Q

what inhibits NF-KB activation?

A

CARD8

31
Q

what mediates the production of Type I interferon?

A

TLR4, TLR9, NOD2

32
Q

the formation of NLRP3 inflammasome results in what?

A

cleavage of pro-IL-1Beta and pro-IL-18 generating a matured form of cytokines

33
Q

what is lactorferrin and what does it do?

A

Fe scavenger/exporter

grabs Fe 2+

34
Q

iNOS converts what to what?

A

Citruline to Arginine

35
Q

what does the NADPH oxidase utilize as a catalyst?

A

SOD (superoxide dimutase)

36
Q

what are bacterial defense mechanisms?

A

modification of their surface
catalase expression, converts reactive species to less harmful compounds
prevention of protein complexes that synthesize RNS or ROS

37
Q

what kind of bacteria uses resistance to phagocytosis as evasion?

A

pneumococcus

Neisseria meningitidis

38
Q

what kind of bacteria uses scavenging of ROS for evasion?

A

catalase-positive staphylococci

39
Q

how does humoral immunity function against extracellular bacteria?

A

block infection, eliminate microbes, neutralize their toxins

40
Q

ABs responses against extracellular bacteria are directed at what?

A

cell wall Ags and secreted cell-associated toxins

41
Q

humoral immunity is the principal mech of defense against what?

A

TI polysaccharide-rich Ags of encapsulated bacteria

42
Q

what Ab may IFN-Gamma stimulate production of?

A

IgGs

43
Q

what is the major injury in response to extracellular bacteria?

A

inflammation and septic shock

44
Q

what causes septic shock?

A

endotoxin released by killed gram + or - extracellular bacteria, caused by cytokines that are produced by macrophages

45
Q

what does TNF-alpha upregulate?

A

Tissue factor (TF) and iNOS

46
Q

what does IL-18 do?

A

induces INF-Gamma –> act. macrophages

47
Q

what cytokines activate neutrophils, lymphocytes and vascular endothelium, upregulate cellular adhesion molecules, induce prostaglandins, etc.

A

IL-1, 6, 12, 15, 18, TNF-alpha, IL-10 (negative regulator)

48
Q

What chemokines mobilize and activate inflammatory cells (neutrophils) and act. macrophages?

A

IL-8, MCP-1, MCP-3

49
Q

what lipid mediators activate vascular endothelium, regulate vascular tone, act. extrinsic coagulation cascade?

A

prostaglandins, leukotrienes

50
Q

what oxygen radicals have antimicrobial properties and regulate vascular tone?

A

superoxide and hydroxyl radicals, NO

51
Q

what do superantigens bind to?

A
class II MHC OUTSIDE the peptide grinding groove
binds variable region of diff. TCR Beta chains regardless of specificty
52
Q

what do superantigens cause?

A

polyclonal T cell activation

53
Q

what are some SAgs in human disease?

A
food poisoning - SEA-SEE and SEG-SEI
Toxic shock syndrome (TSS)
Streoiciccal toxic shock syndrome (STSS)
Acute rheumatic fever (ARF)
Kawaski disease (KD)
Autoimmune diseases
54
Q

what causes TSS, what is the result?

A

S. aureus

capillary leak syndrome

55
Q

what causes STSS, what is it

A

S. pyogenes

most severe form of invasive streptococcal infection

56
Q

what causes ARF?

A

post-infection cause of preventable pediatric heart disease

57
Q

what is KD?

A

acute multi-system vasculitis

58
Q

what is the major mechanism used by bacteria to evade humoral immunity?

A

variation of surface Ags

59
Q

What can activate the alternative or MBL complement system?

what is the result?

A

surface LPS, C-reactive protein

bacterial lysis