Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

CR3

A

binds C3bi- bound complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CR2

A

mainly found on Bcells, involved in their activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CR4

A

similar to CR3, but also adhesion molecule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

development of B lymphocytes

A

steps.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what tests B lymphs when they are graduating?

A

stroma cells, they secrete cytokines at them.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how are histones modified?

A

acetylation- activates, methylation- inactivates.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SCID

A

severe combined immunodeficiency disease

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

type 2 interferons

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what induces liver to produce acute phase proteins?

A

IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

c-reactive protein

A

opsonin, induces phagocytocis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

C3 convertase

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

amplification

A

C3 cleavage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

C5

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

MAC

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

C8 deficiency

A

recurrent Neisseria infections to to lack of MAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

C3 mutations

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

C5 mutations

A

increased complement activation, deplete C3, recurrent infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
MBL
member of the collectin family of proteinsuses specific set of MASP proteasescleaves C4, then C2.
26
Classical C3 convertase
C4bC2b
27
calssical pathway
utilizes bound antibodyneed to bind multiple arms of C1.
28
best antibody for activation of c'
IgM
29
regulation of complement
1. specific activation 2. short half life 3. regulation
30
C1 inhibitor
serine protease inhibitor. SERPIN family. also helps regulate clotting
31
CD59
inhibits formation of MAC, AKA MAC-inhibitory protein
32
Paroxysmal nocturnal hemoglobinuria
missing CD59. complement induced RBC lysis. via random activation of MACs on RBCsacquired. CD59 just goes missing. PIGA - x linked
33
Familial Atypical Hemolytic Uremic Syndrome
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.
34
what is controlled most carefully?
C3 convertase. its generation and stability.
35
which is a most common infection with complement deficiencies?
Neisseria species
36
MIC
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
LAD
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
type 1 interferons
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
type 2 interferons
produced by Nk cells. AKA gamma interferon. Activates Macrophages.
40
what induces liver to produce acute phase proteins?
IL-6
41
acute phase proteins
manose binding lectin, c- reactive protein
42
c-reactive protein
opsonin, induces phagocytocis
43
C' functions
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
C3 convertase
cleaves C3 so that it can tag bacteria for destruction.C3a, part of C3 will then recruit phags AKA C3bBb
45
3 ways that complement is activated
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
C1-9 with 4 out of line.
the classical pathwaylectin pathway doesn't use C1 alternative activates C3 directly.
47
regulation of C3 activation
Factor H+ Factor I- inhibitor, slows down consumption of C3^^^ if missing this then you are more susceptible to encapsulated bacteria.
48
MAC
membrane attack complex. formed by complement, poly 9 forms the pores.
49
C3 mutations
no complement response!!!! !severe, recurrent infections
50
C5 mutations
increased complement activation, deplete C3, recurrent infections.
51
C1inh mutation
angioedema, HAE
52
Classical C3 convertase
C4bC2b
53
best antibody for activation of c'
IgM
54
CR1
major activation receptor for macros and PMNs
55
immune complex disease
lack CR1 or liver receptors inability to clear bloodstream of immune complexeskidney is site of deposition. Nephritis.
56
regulation of complement
1. specific activation 2. short half life 3. regulation
57
C1 inhibitor
serine protease inhibitor. SERPIN family. also helps regulate clotting
58
HAE
Heredetary C1 inhibitor deficiency, angioedema due to overactive complement.
59
CD59
inhibits formation of MAC
60
immunoglobulin gene rearangement
no proliferation during DJ and VDJ rearangement proliferation after successful VDJ rearanement depends on the pre-receptor no proliferation during VJ rearangement
61
lectin pathway
The lectin pathway is homologous to the classical pathway, but with the opsonin, mannose-binding lectin (MBL), and ficolins, instead of C1q.
62
how do A-B type toxins work?
two different ways of entering cells. B- binding site A- toxic part, after T bores out of phagozome.
63
how can bacterial toxins affect host cells and the course of an infection?
they can make bacteria better survive host response.
64
how can toxins be used for treatment?
Botulinum toxin
65
how are toxins inactivated?
antibody, drugs.
66
endotoxin vs exotoxin
endotoxin is LPS, part of bacteria. exotoxin actively secreted to cause disease
67
Necrosis
injury induced, uncoordinated early cell membrane disruption cell swelling cells die in large groups acute inflammation PATHOLOGIC!!!!
68
Apoptosis
Programmed cell death activation of caspade cascade nuclear pyknosis one cell at a time no inflammation normal phneomena
69
coagulative necrosis
with ischemia, makes infarct
70
liquefactive necrosis
loss of substance, in brain or abcess
71
fat necrosis
necrosis in fat
72
casueous necrosis
necrotizing granulomas, combo of liquefactive and coagulative. fungal or TB infection
73
gangrenous necrosis
necrosis of whole anatomical area.
74
leukocytosis with neutrophilia
acute inflammation, left shift, depleted neutros
75
leukocytosis with lymphocytosis
chronic inflammation, viral!
76
eosinophilia
parasitic infection, autoimmune, asthma/allergy, tumors
77
increased sedimentation rate
sign of inflammation, fibrinogen is acute phase. how many RBCs sink in one hour in a vertical capillary tube.
78
steps in tissue healing
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
problems in tissue repair
slow too much- hypertrophic scar, keloid, desmoid too little- wound dehiscence, cardiac rupture after infarct
80
how does antibiotic resistance happen?
antibiotic kills most bugs except resistant ones, resistant bacteria take over, HGT leads to resistance in other bugs!!!
81
mechanisms of resistance to antibiotics
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
how many human infections may involve biofilms?
65%, if you dont count periodontal disease!
83
autoclaves
sterilize equipment with high P and T. 121 degrees for 15 minutes.
84
spores
tough!!!! might not get killed by autoclave, and especially not by hand sanitizers. why? they are dormant. protected.

Host and Defense (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions