Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Host and Defense > Immunology 1.4 C* > Flashcards

Immunology 1.4 C* Flashcards

1
Q

MIC

A

MHC class I-related chain

for infected cells that have had their receptors down regulated by viruses, NK cells recognize these and kill the cell.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
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
4
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
5
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
6
Q

acute phase proteins

A

manose binging lectin,

c- reactive protein

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

c-reactive protein

A

opsonin, induces phagocytocis

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

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

C’ tags are permanent

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

C3 convertase

A

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

AKA C3bBb

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

covalent likage to substrate

A

form a covalent bond, permanently marking it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
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
13
Q

C1-9 with 4 out of line.

A

the classical pathway
lectin pathway doesn’t use C1

alternative activates C3 directly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

amplification

A

C3 cleavage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
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
16
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.

17
Q

C5

A

initiates assembly of membrane attack complex in solution

activated by C5 convertase, activates terminal part of complement

18
Q

MAC

A

membrane attack complex.

formed by complement, poly 9 forms the pores.

19
Q

C8 deficiency

A

recurrent Neisseria infections to to lack of MAC

20
Q

C3 mutations

A

no complement response!!!!!

severe, recurrent infections

21
Q

C5 mutations

A

increased complement activation, deplete C3, recurrent infections.

22
Q

C1inh mutation

A

angioedema

23
Q

MBL

A

member of the collectin family of proteins
uses specific set of MASP proteases
cleaves C4, then C2.

24
Q

Classical C3 convertase

A

C4bC2b

25
Q

calssical pathway

A

utilizes bound antibody

need to bind multiple arms of C1.

26
Q

best antibody for activation of c’

A

IgM

27
Q

CR1

A

major activation receptor for macros and PMNs

28
Q

immune complex disease

A

lack CR1 or liver receptors
inability to clear bloodstream of immune complexes

kidney is site of deposition. Nephritis.

29
Q

regulation of complement

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

C1 inhibitor

A

serine protease inhibitor. SERPIN family.

also helps regulate clotting

31
Q

Hereditary HAE

A

C1 deficiency

32
Q

DAF

A

decay acclerating factor

cell surface membrane of host, dissociates C2b

33
Q

CD59

A

inhibits formation of MAC

34
Q

Paroxysmal nocturnal hemoglobinuria

A

missing CD59

complement induced RBC lysis. via random activation of MACs on RBCs

acquired. CD59 just goes missing.

PIGA - x linked

35
Q

Familial Atypical Hemolytic Uremic Syndrome

A

associated with lack of control of converts activation.

means complement cascade is always activated.

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

36
Q

what is controlled most carefully?

A

C3 convertase. its generation and stability.

37
Q

which is a most common infection with complement deficiencies?

A

Neisseria species

Host and Defense (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions