Antibody Mediated Immune Response Flashcards

1
Q

Ig rearrangement occurs where?

A

bone marrow

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2
Q

What is the main Ag receptor isotype of the surface of most peripheral B cells?

A

IgD often co-expressed with IgM

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3
Q

Some children with periodic fever have increased levels of what?

A

IgD

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4
Q

Before a B cell can leave the bone marrow it must undergo what?

A

central tolerance or negative selection

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5
Q

negative selection prevents what?

A

the development of autoimmunity

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6
Q

the second mechanism for preventing recognition of self-ags?

A

receptor editing

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7
Q

receptor editing consists of?

A

reactivation of Ig gene recombination and expresses new light chain

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8
Q

Activation of B cells by Ag in the lymph node initiates what process:

A
  1. B cell proliferation
  2. B cell increases expression of: Ag (MHC class II), B7 (CD80/CD86), receptors for cytokines produced by Th cell
  3. Secrete low levels of IgM
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9
Q

Where do Ag-activated B cells migrate to within the lymph node?

A

from lymphoid follicle to T cell rich zones of lymph node

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10
Q

Which part of complement is very important at the beginning of infection when amount of microbial Ag is limited?

A

CR2

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11
Q

what does CR2 bind?

A

C3d, a fragment of C3b deposited on bacteria

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12
Q

CR2 does what to B cells?

A

makes B cell very sensitive to Ags

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13
Q

CR2 helping B cells helps to illustrate what concept of immune system?

A

cooperation between innate and adaptive immunity

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14
Q

Ags are processed and peptides produced are presented on what of B cells?

A

class II MHC

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15
Q

T cells activate B cells through?

A

direct contact and cytokines

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16
Q

CD40 is expressed on which cell?

A

B cells

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17
Q

CD40L is expressed on what cell?

A

T helper cells

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18
Q

What must happen with BCRs for the B cell to be activated?

A

cross-linked

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19
Q

what does activation of the B cells result in?

A

proliferation, initial antibody production, germinal center reaction

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20
Q

what is the first antibody produced by B cells?

A

IgM

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21
Q

Ab class is determined by which region?

A

Fc region of heavy chain

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22
Q

During B cell maturation it can switch to produce what?

A

IgG, IgA, or IgE

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23
Q

Principal effector function of IgA

A

mucosal immunity

24
Q

Principal effector function of IgG subclasses (IgG1, IgG3)

A

Fc-dependent phagocyte responses; complement activation; neonatal immunity (placental transfer)

25
Q

Principal effector function of IgM

A

complement activation

26
Q

Principal effector function of IgE

A

immunity against helminths (eosinophil-mediated); mast cell degranulation (immediate hypersensitivity)

27
Q

Mechanism of Ig class switching?

A

intrachromosomal recombination within G-rich tandem repeated DNA sequences called S (switch) regions located upstream of heavy chain constant region genes (except C-delta)

28
Q

High rate of mutation of VDJ gene segments is referred to as?

A

somatic hypermutation

29
Q

Where does somatic hypermutation mutate?

A

part of rearranged gene that encodes Ag-binding domain

30
Q

Somatic hypermutation creates B cells with BCRs?

A

with higher affinity or stimulated more easily because they get Ag first

31
Q

B cells with higher affinity proliferate…?

A

more robust than lower affinity receptors

32
Q

Result of somatic hypermutation?

A

more B cells with higher affinity of BCR for Ag

33
Q

B cells can become what?

A

plasma cell or memory cell

34
Q

plasma cells travel where?

A

spleen or back to bone marrow

35
Q

plasma cells live about how long?

A

5 days

36
Q

Memory seems to be only activated when?

A

CD40-CD40L interaction occurs

37
Q

Thymus-dependent antigen chemical nature?

A

proteins

38
Q

Thymus-independent antigen chemical nature?

A

polymeric antigens, esp. polysaccharrides, glycolipids, nucleic acids

39
Q

Does isotype switching occur with thymus-dependent antigens?

A

Yes

40
Q

Does isotype switching occur with thymus-independent antigens?

A

little or no (may be some IgG)

41
Q

Do antibodies of thymus-dependent antigens have affinity maturation?

A

yes

42
Q

do antibodies of thymus-independent Ags produce secondary response (memory B cells)?

A

Only seen with some antigens

43
Q

What are 3 properties of Thymus-independent Ags?

A
  1. polymeric structure
  2. resistance to degradation (persist for long periods of time and continue to stimulate the immune system)
  3. polyclonal activation of B cells
44
Q

What do TI-Ags do to B cells?

A

cross-link many BCRs

45
Q

TI-1 Ags are?

A

polyclonal activators of B cells

46
Q

What kinds of molecules are normally TI-Ags?

A

Usually polysaccharide lipids and other nonprotein Ags

47
Q

TI-2 Ags are?

A

(not polyclonal) are Ags with repeating epitopes for cross-linking BCRs

48
Q

TI-1 Ags signaling?

A

1: BCR binds Ag
2: TLR
* no CD4 cell help
may be non-specific (e.g. such as LPS)

49
Q

TI-2 Ags signaling?

A

1: BCR binds Ag
2: clustering of BCRs
* no CD4 cell help

50
Q

TI-2 Ag immune responses

A

generated against repetitive Ags

51
Q

B cells activated with TI-2 Ags by?

A

direct BCR cross-linking

52
Q

Does TI-2 Ag immune response produce memory?

A

no

53
Q

For TI-2 Ags what kind of Ab produced?

A

mostly IgM

54
Q

Abs produced in response to TI-2 Ags had what kind of affinity?

A

relative low

55
Q

What kind of belong to TI Ags?

A

many bacterial cell wall polysaccharides

56
Q

What are the advantages of TI-Ags?

A

B cells can be activated right away without T cells activated

57
Q

Patients with congenital or acquired deficiencies of Ab-mediated response are susceptible to infections of what?

A

encapsulated bacteria