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Host and Defense > Review 1.2 > Flashcards

Review 1.2 Flashcards

1
Q

CR1

A

complement receptor 1

binds C3b and C4b

major activator receptor for macros and PMNs

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2
Q

CR3

A

binds C3bi- bound complexes

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3
Q

CR2

A

mainly found on Bcells, involved in their activation

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4
Q

CR4

A

similar to CR3, but also adhesion molecule.

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5
Q

development of B lymphocytes

A

steps.

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6
Q

RAG

A

encode enzymes that play an important role in the rearrangement and recombination of the genes of immunoglobulin and T cell receptor molecules during the process of VDJ recombination.

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7
Q

what tests B lymphs when they are graduating?

A

stroma cells, they secrete cytokines at them.

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8
Q

how are histones modified?

A

acetylation- activates, methylation- inactivates.

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9
Q

SCID

A

severe combined immunodeficiency disease

gamma chain deficiency- cytokine receptor. shared by IL-2 family of receptors.

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10
Q

type 1 interferons

A

antiviral response that results in cells having a higher level of resistance to infection than unactivated cells.response driven by JAC STAT pathway.Main effect: resistance of viral replication, and infection.recognized by NK cells.

immunomodulatory.

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11
Q

type 2 interferons

A

produced by Nk cells. AKA gamma interferon. Activates Macrophages.

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12
Q

what induces liver to produce acute phase proteins?

A

IL-6

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13
Q

c-reactive protein

A

opsonin, induces phagocytocis

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14
Q

C’ functions

A

opsonization and phagocytocis- binds C3b, recognized by phagocyte, then its eaten.stimulation of inflammatory reactions- recruits and activates leukocytes by C5a and C3acomplement mediated cytolysis- recruits components, forms pore, osmotic lysis of microbe.

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15
Q

C3 convertase

A

cleaves C3 so that it can tag bacteria for destruction.C3a, part of C3 will then recruit phagsAKA C3bBb

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16
Q

3 ways that complement is activated

A

Classical - least important.

Lectin - activated by acute phase proteins. has to go to liver first.

Alternative - doesn’t need antibody, most important. first to act.

they all lead to cleavage of C3 to C3a and b. C3b can also cleave C3 to make more C3a

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17
Q

amplification

A

C3 cleavage

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18
Q

Alternative pathway

A

main way to activate complement. C3 cleavage driven by:

Factor B- forms C3bBb complex aka C3 convertase

Factor D- cleaves B when bound to C3b to Ba and Bb

Properdin- stabilizes complexes formed by other factors. positive regulator. accelerator.

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19
Q

regulation of C3 activation

A

Factor H+ Factor I- inhibitor, slows down consumption of C3^^^ if missing this then you are more susceptible to encapsulated bacteria.

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20
Q

C5

A

initiates assembly of membrane attack complex in solutionactivated by C5 convertase, activates terminal part of complement

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21
Q

MAC

A

membrane attack complex. formed by complement, poly 9 forms the pores.

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22
Q

C8 deficiency

A

recurrent Neisseria infections to to lack of MAC

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23
Q

C3 mutations

A

no complement response!!!!!severe, recurrent infections

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24
Q

C5 mutations

A

increased complement activation, deplete C3, recurrent infections.

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25
Q

MBL

A

member of the collectin family of proteinsuses specific set of MASP proteasescleaves C4, then C2.

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26
Q

Classical C3 convertase

A

C4bC2b

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27
Q

calssical pathway

A

utilizes bound antibodyneed to bind multiple arms of C1.

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28
Q

best antibody for activation of c’

A

IgM

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29
Q

regulation of complement

A
  1. specific activation 2. short half life 3. regulation
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30
Q

C1 inhibitor

A

serine protease inhibitor.

SERPIN family.

also helps regulate clotting

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31
Q

CD59

A

inhibits formation of MAC, AKA MAC-inhibitory protein

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32
Q

Paroxysmal nocturnal hemoglobinuria

A

missing CD59.
complement induced RBC lysis. via random activation of MACs on RBCsacquired. CD59 just goes missing.

PIGA - x linked

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33
Q

Familial Atypical Hemolytic Uremic Syndrome

A

associated with lack of control of convertase activation. means complement cascade is always activated.

missing Factor H, factor I, mutation in C3, increased C3 consumption.

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34
Q

what is controlled most carefully?

A

C3 convertase. its generation and stability.

35
Q

which is a most common infection with complement deficiencies?

A

Neisseria species

36
Q

MIC

A

MHC class I-related chainfor infected cells that have had their receptors down regulated by viruses, NK cells recognize these and kill the cell.

37
Q

LAD

A

leukocyte adhesion deficiency:

inability of leukocytes to migrate into sites of infection: history of overwhelming infections. often lethal.

early symptom:
** delayed loss of umbilical cord***
no PMNs and macros in sites of infection.higher levels in blood.

38
Q

type 1 interferons

A

antiviral response that results in cells having a higher level of resistance to infection than unactivated cells.

response driven by JAC STAT pathway.

Main effect: resistance of viral replication, and infection.

recognized by NK cells.immunomodulatory.

39
Q

type 2 interferons

A

produced by Nk cells. AKA gamma interferon. Activates Macrophages.

40
Q

what induces liver to produce acute phase proteins?

A

IL-6

41
Q

acute phase proteins

A

manose binding lectin, c- reactive protein

42
Q

c-reactive protein

A

opsonin, induces phagocytocis

43
Q

C’ functions

A

opsonization and phagocytocis- binds C3b, recognized by phagocyte, then its eaten.

stimulation of inflammatory reactions- recruits and activates leukocytes by C5a and C3a

complement mediated cytolysis- recruits components, forms pore, osmotic lysis of microbe.

44
Q

C3 convertase

A

cleaves C3 so that it can tag bacteria for destruction.C3a, part of C3 will then recruit phags AKA C3bBb

45
Q

3 ways that complement is activated

A

Classical - least important.
Lectin - activated by acute phase proteins. has to go to liver first.

Alternative - doesn’t need antibody, most important. first to act. they all lead to cleavage of C3 to C3a and b. C3b can also cleave C3 to make more C3a

46
Q

C1-9 with 4 out of line.

A

the classical pathwaylectin pathway doesn’t use C1 alternative activates C3 directly.

47
Q

regulation of C3 activation

A

Factor H+ Factor I- inhibitor, slows down consumption of C3^^^ if missing this then you are more susceptible to encapsulated bacteria.

48
Q

MAC

A

membrane attack complex. formed by complement, poly 9 forms the pores.

49
Q

C3 mutations

A

no complement response!!!!

!severe, recurrent infections

50
Q

C5 mutations

A

increased complement activation, deplete C3, recurrent infections.

51
Q

C1inh mutation

A

angioedema, HAE

52
Q

Classical C3 convertase

A

C4bC2b

53
Q

best antibody for activation of c’

A

IgM

54
Q

CR1

A

major activation receptor for macros and PMNs

55
Q

immune complex disease

A

lack CR1 or liver receptors inability to clear bloodstream of immune complexeskidney is site of deposition. Nephritis.

56
Q

regulation of complement

A
  1. specific activation 2. short half life 3. regulation
57
Q

C1 inhibitor

A

serine protease inhibitor.

SERPIN family.
also helps regulate clotting

58
Q

HAE

A

Heredetary C1 inhibitor deficiency, angioedema due to overactive complement.

59
Q

CD59

A

inhibits formation of MAC

60
Q

immunoglobulin gene rearangement

A

no proliferation during DJ and VDJ rearangement

proliferation after successful VDJ rearanement depends on the pre-receptor

no proliferation during VJ rearangement

61
Q

lectin pathway

A

The lectin pathway is homologous to the classical pathway, but with the opsonin, mannose-binding lectin (MBL), and ficolins, instead of C1q.

62
Q

how do A-B type toxins work?

A

two different ways of entering cells.

B- binding site

A- toxic part, after T bores out of phagozome.

63
Q

how can bacterial toxins affect host cells and the course of an infection?

A

they can make bacteria better survive host response.

64
Q

how can toxins be used for treatment?

A

Botulinum toxin

65
Q

how are toxins inactivated?

A

antibody, drugs.

66
Q

endotoxin vs exotoxin

A

endotoxin is LPS, part of bacteria.

exotoxin actively secreted to cause disease

67
Q

Necrosis

A

injury induced, uncoordinated

early cell membrane disruption

cell swelling

cells die in large groups

acute inflammation

PATHOLOGIC!!!!

68
Q

Apoptosis

A

Programmed cell death

activation of caspade cascade

nuclear pyknosis

one cell at a time

no inflammation

normal phneomena

69
Q

coagulative necrosis

A

with ischemia, makes infarct

70
Q

liquefactive necrosis

A

loss of substance, in brain or abcess

71
Q

fat necrosis

A

necrosis in fat

72
Q

casueous necrosis

A

necrotizing granulomas, combo of liquefactive and coagulative.

fungal or TB infection

73
Q

gangrenous necrosis

A

necrosis of whole anatomical area.

74
Q

leukocytosis with neutrophilia

A

acute inflammation, left shift, depleted neutros

75
Q

leukocytosis with lymphocytosis

A

chronic inflammation, viral!

76
Q

eosinophilia

A

parasitic infection, autoimmune, asthma/allergy, tumors

77
Q

increased sedimentation rate

A

sign of inflammation, fibrinogen is acute phase.

how many RBCs sink in one hour in a vertical capillary tube.

78
Q

steps in tissue healing

A

inflammatory response, clotting factors leak in.

clot forms

fibroblasts and others cells migrate in, form granulation tissue

maturation of granulation tissue

scar maturation- 70-75% strength after months

79
Q

problems in tissue repair

A

slow

too much- hypertrophic scar, keloid, desmoid

too little- wound dehiscence, cardiac rupture after infarct

80
Q

how does antibiotic resistance happen?

A

antibiotic kills most bugs except resistant ones, resistant bacteria take over, HGT leads to resistance in other bugs!!!

81
Q

mechanisms of resistance to antibiotics

A

drug cant get it, drug gets pumped out, drug gets inactivated, target is altered or over-expressed so that drug can’t affect it.

82
Q

how many human infections may involve biofilms?

A

65%, if you dont count periodontal disease!

83
Q

autoclaves

A

sterilize equipment with high P and T.

121 degrees for 15 minutes.

84
Q

spores

A

tough!!!!

might not get killed by autoclave, and especially not by hand sanitizers.

why? they are dormant. protected.

Host and Defense (22 decks)

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