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HDM Exam #2 > Humoral Immune Responses > Flashcards

Humoral Immune Responses Flashcards

1
Q

Primary immune response

A

Naive B cells are stimulated by Ag, become activated and differentiate into plasma cellsthat produce Abs (IgM>IgG).

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2
Q

Secondary immune response

A

Response elicited when the same Ag stimulates memory cells leading to the production of Abs (IgG>IgM).

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3
Q

Follicular B cells

A

Respond to protein Ags and initiate T cell dependent Ab responses.

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4
Q

MZ B cells

A

Respond to multivalent Ags and are T cell independent.

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5
Q

B-1 cells

A

In mucosal sites. Respond to multivalent Ags and are T cell independent.

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6
Q

B-2 cells overview

A

Widely distributed.
Continually replaced by bone marrow..
Require interaction with T cells for activation and proliferation.

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7
Q

B-1 cells overview

A

Arise from fetal liver.
May represent bridge between innate and adaptive immune system.
B-1 Abs are often directed against conserved microbial Ags.

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8
Q

CXCL13 function

A

Secreted by FDCs and guides the movement of B cells into the follicle of the LN.

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9
Q

Most Ags from the tissues are transported to LNs via:

A

Afferent lymphatic vessels that drain into the subscapular sinus of the LNs.

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10
Q

Soluble Ags:

A

May reach the B cell zone of the follicle and interact directly w/ specific B cells.

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11
Q

Large Ags:

A

May be captured by resident FDCs and transported into follicles where they activate B cells.

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12
Q

Microbes and Ag-Ab complexes:

A

Are captured by subscapular sinus Mo which deliver Ags to follicles.

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13
Q

Unique function of FDCs:

A

Can retain Ag-Ab complexes on their surface for weeks to months.

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14
Q

Ag retention by FDCs is mediated by:

A

FC receptors, CR 1 or CR 2 complement receptors.

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15
Q

FDCs do not:

A

Express MHC II OR phagocytose and process exogenous Ags for MHC I.

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16
Q

Cells in the marginal zone (2):

A

MZ Mo.

MZ B cells.

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17
Q

MZ B cells in the spleen can:

A

Bind immune complexes containing Ag and are coated in complement using complement receptors in a manner that is independent of BCR specificity.
MZ B cells can now shuttle to follicular region.
In the follicular region, FDCs can compete to bind to the Ag.
MZ B cells then migrate back to the marginal zone.

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18
Q

Ag capture in the spleen:

A

Ags usually presented to MZ B cells in native conformation.
Ags in immune complexes may bind to CR2 on MZ B cells.
MZ B cells can transfer the complex to FDCs.

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19
Q

What captures blood-borne pathogens?

A

pDCs in the blood and transport them to spleen and deliver to MZ B cells.

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20
Q

What captures polysaccharide Ags in the spleen?

A

MZ Mo and displayed for MZ B cells.

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21
Q

BCR anatomy

A

Transmembrane molecule that expressed IgM/D in naive form.

Signaling is via Ig-alpha and Ig-beta, which are connected by disulfide linkage and contain ITAMs.

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22
Q

B cell coreceptors

A

Associate with BCR complex and enhance or inhibit signal.

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23
Q

CD19

A

Dominant signaling component of B cells

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24
Q

CD21

A

AKA CR2. When combined with CD19, positively regulates B cell activation and lowers threshold for B cell activation.

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25
Q

CD32

A

Contains ITIM nad negatively regulates BCR signaling.

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26
Q

Signaling mechanism of BCR complex (4)

A
  1. Ag binding causes conformational change in ITAMs, making them accessable to Src kinases (Lyn, Fyn, Blk).
  2. Src kinases phosphorylate ITAMs of Ig-alpha/Ig-beta.
  3. Phosphorylated ITAMs allow space for Syk tyrosine kinase, which phosphorylates a Tyr residue on BLNK.
  4. Follows with recruitment of enzymes which actiavte Ras and Rac, PLCy2 and Btk.
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27
Q

CD81

A

Complexes with CD21 and CD19 and is necessary for normal CD19 expression.

28
Q

C3d

A

Fragment of C3b that remains on the microbial surface after C3b is degraded. Binds to CD21/CR2.

29
Q

The complex of C3d and Ag interacts with the B cell how?

A

The Ag binds to the BCR and CR2/CD21 recognizes C3d.

30
Q

B cell coreceptor components

A

CR2/CD21-CD19-CD81

31
Q

How does CD19 enhance the amplification of BCR signaling?

A

Tail of CD19 becomes phosphorylated and recruits Lyn kinases which can phsophorylate ITAMs in Ig-alpha and Ig-beta..

32
Q

Mechanism of T cell mediated activation of B cell

A

When Th cells become activated by binding Ags presented on B cells, they express CD40L.
CD40L binds to CD40 on B cells and stimulates B cell proliferation.

33
Q

Upon B-T cell inteaction:

A

B cells produce short-lived plasma cells mainly producing IgM.
B cells then migrate to GC and undergo somatic mutation, affinity maturation, isotype switching and generation of memory B cells and long lived plasma cells.

34
Q

Generation of Tfh requires:

A

Sequential activation of T cells, first by DCs ad then activated B cells. Tfh migate into GCs where they activate B cells.

35
Q

IL-21 is secreted by Tfh cells because:

A

It is required for GC development and generation of plasma cells.

36
Q

Tfh secrete IFN-y or IL-4 because:

A

It controls isotype Th1 or Th2 switching.

37
Q

Tfh express (4):

A

ICOS
PD-1
IL-21
Bcl-6

38
Q

IL-21 and B cells

A

IL-21 is important for generation of B cell responses in GCs.

39
Q

Dark zone of GC

A

Formed by activated B cells migrating back into the follicle and proliferating. These cells undergo extensive isotype switching and somatic hypermutation,

40
Q

Light zone of GC

A

Formed by the area that B cells encounter with FDCs.

41
Q

Where do plasma cells and memory cells live?

A

Plasma cells live in BM and memory B cells return to the recirculating lymphocyte pool.

42
Q

Isotype switching occurs in:

A

The GCs and is driven by Tfh cells.

The variable chains is unaltered, but the constant regions of the heavy chains are altered.

43
Q

IFN-y (Th1) induces what kind of switching?

A

IgG swithcing

44
Q

IL-4 (Th2) induces what kind of switching?

A

IgE swithcing

45
Q

Switching sequence

A

Precedes C gene and controls rearrangement process.

46
Q

Affinity maturation is only found in:

A

Ab responses to T cell dependent Ags.

47
Q

There are more mutations in IgG than:

A

IgM

48
Q

Class-switch recombination

A

Occurs in activated B cells and changes Cm gene to another CH gene.
Takes place between 2 switch regions (S) and results in a looped out deletion of DNA.
Causes a switch from IgM/IgD to IgA/G/E, etc.

49
Q

Affinity maturation leads to:

A

Increased affinity of Abs for an Ag.

50
Q

What is required for somatic hypermutation of Ig V genes?

A

Tfh cells and CD40:CD40L interactions.

51
Q

How are B cells “chosen” in the in the GC?

A

In dark zone, Ag specific B cells are produced. The cells with the most affinity for an antigen presenting FDC proliferates, and the others undergo apoptosis.

52
Q

Where are mutations from affinity maturation clustered?

A

In the V regions, mostly in the Ag-binding complementary-determining regions.

53
Q

Why is the GC considered the B cells’ graveyard?

A

Because of somatic hypermutation and affinity maturation that occur there causing an increase in apoptosis.

54
Q

Mechanism of B cell survival:

A

Cells that have undergone somatic hypermutation enter the light zone of the GC to interact w/ FDCs.

  1. Ag recognition induces expression of Bcl-2, an anti-apoptotic protein.
  2. High-affinity B cells will endocytose and present for Tfh cells in the GC which signals CD40L to promote B cell survival.
  3. High-affinity B cells may also activate inhibitors of Fas once they recognize Ag.
55
Q

B cell lymphomas develop in:

A

Germinal centers.

DNA breaks in somatic hypermutation and isotype switching can facilitate incorporation of oncogenes.

56
Q

Memory B cells express high levels of what?

A

Bcl-2 (anti apoptotic)

57
Q

T independent

A

Some non-protein Ags can elicit Ab production without access to Th cells. They are T independent.
The Abs produced are usually low affinity, consist mainly of IgM and have limited isotype switching.
MZ B cells are mainly involved.

58
Q

Most TI Ags are:

A

Multivalent. Usually bind to IgM.

Induce maximal cross-linking of the BCR and lead to activation without a Th.

59
Q

TI Ags cannot be recognized by:

A

MHC molecules and are not recognized by CD4+.

60
Q

Some TI Ags can induce:

A

Isotype switching, which can be enhanced by release of cytokines from non T cells.

61
Q

In humans the dominant Ab class induced by pneumococcal capsular polysaccharide is:

A

IgG2

62
Q

IGF-beta can help mediate what?

A

Switch to IgA. It is secreted by non-lymphoid cells at mucosal sites.

63
Q

Memory from vaccines occurs only if:

A

The vaccine can activate Th cells.

64
Q

Vaccines for capsular polysaccharides do not stimulate memory because:
How do we get around this?

A

They don’t stimulate Th cells.

The polysaccharide is linked to a foreign protein to forma hapten-carrier conjugate (conjugate vaccine).

65
Q

Inhibitor signaling in lymphocytes

A

Ligand binding of ITIM causes its phosphorylation by Src kinase.
The phosphorylated ITIMs recruit tyrosine phosphatases which attenuate immune signaling.

66
Q

How does FcyRIIB (CD31) affect signaling?

A

The Ag-Ab complex can bind to both the BCR and FcyRIIB via the Fc portion of the Ab. The FcyRIIB can activate phosphatases which inhibit the signaling.

67
Q

SHP and SHIP are:

A

Phosphatases recruited by ITIMs.

HDM Exam #2 (7 decks)

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