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Flashcards in Immunology Deck (80):
1

koch's modified postulates (3)

phenotype under study associated w pathogenic strain
inactivation of virulence genes leads to loss of virulence
reversion/replacement of mutated genes restores pathogenicity

2

considerations for disease (5)

virulence factors, number of organisms present, host defenses, attenuation, avirulence

3

examples of virulence factors

capsule, pilli, toxins

4

avirulent

can no longer cause disease

5

in order for a microbe to cause disease, it must (5)

get inside the host, attach to specific cells/tissues, evade host defense, get nutrients, and exit the host

6

antigen variation

change VSG surface proteins

7

antigen variation in Trepanosoma brucei

has over 10,000 variants; as immune response builds up to one, VSG proteins change, immune system needs to make new response

8

AB toxin subunits

A subunit is active, B subunit binds

9

Shiga toxin

B subunit binds to RNA, A subunit cleaves it - inhibits ribosome activity

10

genus clostridium classification

gram positive rods, endospore forming, obligate anaerobes

11

why do people with botulism smell bad

c. botolinum gets nutrients by fermentation of amino acids - byroducts are ammonia, hydrogen sulfide, fatty acids, etc.

12

botulin toxin is what type of toxin

AB neurotoxin

13

neurotoxin

botulin - flaccid paralysis, muscles can't contract

14

SNARE complex

synaptobrevin in vesicle membrane, syntaxin in cell membrane of neuron, snap 25 binds to each

15

SNARE complex and botulinum

toxin binds receptor on neuron, A subunit cleaves snap 25 - ACH not released into synapse so muscles stay relaxed

16

ACH

utilizes SNARE complex to be released into synapse; binds receptors on muscle cell to cause muscle contraction

17

how does c. botulinum enter and exit the body

ingestion of spore, exits via feces

18

where are c. tetani spores

dust

19

early symptoms of tetanus

restlessness, irritability, jaw muscle contraction

20

late symptoms of tetanus

increased pain, arching of back, difficulty breathing

21

tetanosporin toxin

AB toxin - B subunit binds receptor on motor neuron, travels through CNS to inhibitory neuron, B subunit cleaves synaptobrevin

22

why does tetanosporin cause tetanus symptoms

synaptobrevin cleaved, GABA and glycine can't be released to inhibity motor neuron - motor neuron continually released ACH - muscle contraction

23

tetanus vaccine

antitoxin - the antibody produced binds to the B subunit to prevent the toxin from being taken up

24

whats strange about tetanus

recovery doesn't provide immunity

25

immunology

study of how immune system fxns in the body to prevent/destroy foreign material

26

innate immunity

non-specific, non-adaptive, general response that doesn't require previous exposure

27

innate immunity includes

physical barriers, chemiccal barriers, normal microbiota

28

non-specific recognition of innate immunity

capsid, peptidoglycan, LPS, flagella, pilli, etc.

29

adaptive immunity

occurs after previous exposure, acquired, specific - retains memory after antigen exposure and gets faster/ more specific with each subsequent exposure

30

hematopoesis

make blood from pluripotent hematopoetic stem cells (HSC)

31

HSC differentiates into

lymphoid cells or myeloid cells

32

lymphoid cells differentiate into

natural killer cells, B cells, T cells

33

lymphocytes

B cells and T cells

34

myeloid cells differentiate into

RBCs, mast cells, myeloblast, monoblast

35

myeloblast differentiate into

eosinophils, basophils, neutrophils

36

monoblasts differentiate into

macrophages, dendritic cells

37

whats special about macrohphages and dendritic cells

crossover between innate and adaptive immunity

38

what allows for specificity of B and T cells

receptors

39

phagocytic cells in blood

neutrophils and monocytes

40

monocytes differentiate into

macrophages and dendritic cells

41

phagocytic cells in tissues

macrophages and dendritic cells

42

granulocytes

neutrophils, basophils, eosinophils

43

neutrophils

majority of WBCs, first responders in immune response

44

anti-gen presenting cells

monocytes, macrophages, dendritic cells

45

eosinophils

active in parasitic worm infections; binds to IgE antibodies

46

both eosinophils and basophils

release toxin chemicals to destroy cells, are associated w allergic rxns

47

natural killer cells

destry virally infected or cancerous cells

48

how do natural killer cells detect targets

absence of MHC

49

B cells

produce antibodies

50

T cells

specify immune response (helper and cytotoxic T cells)

51

mast cells

produce histamine

52

classic inflammation

heat, pain, swelling, redness, reduced function

53

phagosome

endocytic vesicle from endocytosing a pathogen

54

phagolysosome

phagosome that had fused with a lysosome

55

opsonization

to make yummy - coat pathogen with antibodies for better detection

56

arms

part of antibody that recognizes antigens

57

Fc

fragment constant region - part of antibody that binds Fc receptors on phagocyte cell membrane

58

primary lymphoid organs

where lymphocytes are made/mature (thyroid for T cells, bone marrow for B cells)

59

secondary lymphoid organs

where antigens are encountered - speen, lymph node, tonsils, etc.

60

mast cells in inflammatory response

dump histamine - vasodilation - fluid and neutrophils can leak out of vessels (pain and swelling)

61

macrophages in inflammatory response

bind pathogens, release cytokine and chemokine

62

cytokine

relay messages between cell types

63

chemokine

provides path for neutrophils to follow from blood vessel to site of infection

64

CAM receptor

cellular adhesion molecules

65

inflammatory response and CAM receptors

upregulation of CAM - neutrophils bind to these receptors on wall of vessel - allow for WBCs to leak out upon vasodilation

66

extravasion

cells leaving blood vessels

67

PAMPs

pathogen associated molecular patterns - molecules on surface of foreign things but not self cells

68

examples of PAMPs

LPS, peptidoglycan, envelope proteins, flagellar proteins, pilli

69

f-Met

bacterial methionine - a very good PAMP

70

how are PAMPs recognized

PRRs - pattern recognition receptors on self cells that recognize non-specific foreign traits

71

why are PRR and PAMP interactions important for immune system

allow for pathogen recognition without opsonization (need for antibodies) - sinze won't have antibodies if initial exposure

72

TLRs

toll-like receptors, form of PRR, recognizes PAMP ligands and leads to signalling pathway and transcription in self cells

73

TLR4

recognizes LPS

74

adaptive immunity divided into

humoral and cellular immunity

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humoral immunity

involves B cells - responds to extracellular pathogens

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cellular immunity

invovles T cells - responds to intracellular pathogens

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helper T cells

CD4+

78

cytotoxic T cells

CD8+

79

B cells and antigen

grab their own antigen

80

T cells and antigen

utilizes antigen presenting cells