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Foundations Exam 2 > B Cells and Antibodies > Flashcards

B Cells and Antibodies Flashcards

1
Q

why are antibodies considered a dimer of dimers

A

two heavy chains that are the same, two light chains that are the same

light chains are shorter, only found in Fab region that binds antibody

both binding sites (each extension of the Y shape) are the same

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2
Q

which of these is true:
a. different antibodies can bind to different epitopes on the same antigen
b. different antibodies can bind to the same epitope on an antigen

A

both true!

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3
Q

part of the antibody that contacts that antigen

A

CDRs (complementary determining regions)

region that shows great variability to increase immune diversity (via VDJ recombination)

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4
Q

____ portion of antibodies controles effector functions such as complement binding

A

Fc portion - various isotypes that can be changed via class switching (IgM/G/A/E/D)

*note that during isotype switching, only Fc (NOT Fab region) changes

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5
Q

what are the isotypes/classes of antibodies and their specialization?

A

IgM: main antibody in primary response, BEST at fixing complement, monomer form is naive BCR (IgD), pentamer held by J chain

IgG: main blood antibody in secondary response, neutralizes toxins/opsonization/fixes complement, CAN cross placenta, binds phagocytes

IgA: secreted in mucus/tears/saliva, can be monomer, highly abundant in gut/mucosal surfaces

IgE: allergy and anti-parasitic responses, binds mast cells and basophils

IgD: naive BCR (function unknown)

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6
Q

T/F: each B cell expresses only one BCR specificity

A

TRUE

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7
Q

4 ways antibodies cause humoral immune response:

A
  1. neutralization: bind pathogen or toxin and prevent its effect
  2. opsonization: antibodies coat antigen, induce phagocytosis
  3. ADCC: antibody-dependent cellular cytotoxicity
  4. complement activation
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8
Q

opsonization works by antibodies binding ____ on phagocytes

A

antibodies coat antigen

antibodies bind Fc receptors on phagocytes

phagocytosis is induced

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9
Q

IgG1 and IgG3 are very good at

A

opsonization

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10
Q

IgM and IgG1/3 are really good at

A

activating complement system

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11
Q

____ antibodies are really good at inducing activation of mast cells

A

IgE: involved in allergy and anti parasitic responses

Fc binds mast cells and basophils

shaped like IgG but more flexible

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12
Q

which Ig isotype can cross the placenta? what are other features of this class?

A

IgG: CAN cross placenta, very good at activating complement system

main blood antibody of secondary response, Fc binds phagocytes

5 subtypes

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13
Q

which type of antibody is found in gut and mucosal surfaces

A

IgA: secreted in mucus, tears, saliva

can be a monomer

has secretary component secreted by epithelial cells that allows transport across epithelial cells in the gut

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14
Q

which antibody class is best for activating the complement system?

A

IgM: main antibody in primary response

monomer is naive BCR (IgD)

J chain holds pentamer together

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15
Q

which occurs first in B cell development, heavy or light chain recombination?

A

heavy chain recombination,
then light chain recombination

2 checkpoints during BCR assembly occur during after IgH gene rearrangement and IgL gene rearrangement

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16
Q

immature B cells all begin with this type of antibody on its surface

A

IgM

class switching occurs later

(also all have IgD on surface, function unknown)

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17
Q

receptor editing in BCR development

A

in bone marrow, BCR that react too strongly to self are signaled for apoptosis

HOWEVER, they are given a “second chance” by another round of light chain rearrangement

if this succeeds, B cell moves to periphery and matures

**note that sometimes self-reactive BCR will sneak through, and peripheral tolerance is required to catch these (either apoptosis or anergy ensues)

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18
Q

what happens to mature B cells that recognize self antigen with high affinity in peripheral tissues in absence of Th?

A

peripheral tolerance mechanisms shut them down, either through:
a. apoptosis
b. anergy (functionally inactive)
c. inhibitory regulation, such as by CD22

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19
Q

what are the 2 types of B cell activation? and the 2 types of B cells involved in these?

A
  1. CD4 T cell/thymus dependent: Follicular B cells responds to protein antigens
  2. T/thymus independent: Marginal zone B cells respond to microbial constitutes (like bacterial polysaccharides) antigens - antigens usually contain repetitive patterns that cross link BCR
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20
Q

Follicular vs marginal zone B cells

A

follicular: CD4 T cell dependent, bind protein antigens

marginal zone: T cell independent, bind microbial antigens with repetitive patterns that cross link BCR

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21
Q

for follicular B cells (T-dependent), activation requires 2 signals:

A
  1. cross linking of BCR - either directly (polyvalent antigen), indirectly (APC), or through alternative complement pathway
  2. CD4 T cell help via CD40-CD40L interaction (essential), mediated by MHC II APC
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22
Q

what are the 3 ways in which T-dependent (follicular) B cells can cross link BCR? (first required signal for activation)

A
  1. directly - polyvalent antigens (+1 copy of specific epitope)
  2. APC presents antigen - monovalent antigens
  3. alternative complement pathway
23
Q

4 consequences of BCR cross-linking? (first signal of T-dependent/follicular B cell activation)

A
  1. increased survival/ proliferation
  2. increased B7 expression (promotes T cell interaction)
  3. increased expression of cytokine receptors (promotes T cell interaction)
  4. increased expression of CCR7 and migration from follicle to T cell areas
24
Q

describe signal 2 of T-dependent (follicular) B cell activation

A

signal 1 is BCR cross-linking

signal 2 is CD40-CD40L interaction between CD4 T cell and B cell (MHC II mediated)

only get B cell activation when you have T cell specific for the same antigen

TFH (T follicular helper T cells): special subset of CD4 Th that provide second signal to follicular B cells

25
Q

describe 1st and 2nd phase of follicular (T-dependent) B cell response

A

1st: activation, proliferation, burst of low affinity Ag-specific Ab —> plasma cells develop that secrete Ab (mostly IgM, reside in lymphoid tissues 3-5 days)

2nd: activated B cells traffic into lymphoid follicles and form germinal centers —> isotype switching, affinity maturation —> produce long-lived plasma cells and memory B cells

26
Q

germinal center response

A

second phase of follicular (T-dependent) B cell activation, when activated B cells traffic into lymphoid follicles and form germinal centers

outcomes: affinity maturation (high affinity antibodies, aka somatic hypermutation), isotype switching, generation of memory B cells, long-lived plasma cells (migrate to bone marrow)

27
Q

how does affinity maturation of B cells occur?

A

aka somatic hypermutation: during germinal center reaction, somatic mutation of Ig V genes and selection of mutated B cells with high-affinity antigen receptors results in production of high affinity antibodies

mutations inserted in part of antibody that directly contacts antigen

28
Q

what 4 tests do follicular B cells need to pass in the germinal centers during affinity maturation?

A
  1. take up sufficient antigen from follicular DC
  2. process/present antigen in context of MHC II
  3. efficiently interact with T follicular Th cells
  4. receive signals from T cells that allow high affinity B cell survival
29
Q

what is the role of AID and mutator in follicular B cell affinity maturation?

A

AID (activation-induced deaminase): necessary for both isotype switching and affinity maturation

mutator: somatic hypermutation causes development of high affinity B cells (turned on in B cells by CD40 ligation)

30
Q

which types of B cells can undergo isotype switching and affinity maturation

A

Follicular (T-dependent)

Marginal zone B cells do NOT undergo isotype switching or affinity maturation - mainly IgM, short-lived

31
Q

what 2 signals are required for marginal zone (T-independent) B cell activation

A

usually respond to polyvalent antigens that can directly cross-link BCR

  1. BCR
  2. TLR activation
32
Q

which respond first to infection, marginal zone or follicular B cells?

A

marginal zone (T-independent) occurs first, followed by follicular B cells

later follicular B cells that have undergone germinal center response take over

33
Q

what changes from primary to secondary antibody response?

A
  • larger peak response
  • more IgG than IgM
  • higher affinity
  • only protein antigens can induce secondary response (because now follicular B cells are leading response)
34
Q

match with antibody response:
bacterial toxins
bacteria in extracellular space
bacteria in plasma

with

complement activation
neutralization
opsonization

A

bacterial toxins —> neutralization

bacteria in extracellular space —> opsonization

bacteria in plasma —> complement activation

35
Q

affinity vs avidity

A

affinity: strength of SINGLE antibody-antigen interaction
—> example: each IgG typically has high affinity for target

avidity: strength of ALL interactions combined
—> example: IgM has low affinity binding but 10 of them has high overall strength of binding

36
Q

isotype vs allotype vs idiotype

A

isotype: classes of antibodies, different constant regions encoded by genes

allotype: allelic differences in antibodies

idiotype: differences in the variable region of antibodies that will ALWAYS vary from individual to individual and antibody to antibody

37
Q

why are allotype and idiotype differences relevant in monoclonal antibody treatment?

A

immune system will recognize allotypic and idiotypic differences and may try to clear the therapeutic mAbs

38
Q

when an immune response occurs in a lymph node, dividing B cells are located in:

A

germinal centers

39
Q

antibody classes differ in their

A

heavy chain CONSTANT regions

40
Q

in which of these will all immunoglobulin molecules be identical?
a. IgG from a single person
b. Fc fragments of IgG form a single person
c. IgG produced by a single plasma cell

A

c. IgG produced by a single plasma cell —> has undergone somatic recombination (so permanent point mutations)

41
Q

Ig___ is present in colostrum

A

IgA

42
Q

Ig___ would be produced in Peyer’s Patches

A

Peyer’s Patches are in small intestine

IgA is produced there

43
Q

antibody with highest concentration in the plasma

A

IgG

44
Q

Ig__ is synthesized by the fetus in response to in utero infection

A

IgM

synthesized by fetus

45
Q

Ig__ is most effect class for agglutination

A

IgM

46
Q

antibodies to ABO antigens are in Ig__ class

A

IgM

47
Q

plasma antibody that can both opsonize and activate complement

A

IgG

48
Q

pathogen-specific antibodies of Ig__ indicate recent infection

A

IgM (primary response - no class switching yet)

49
Q

Ig__ contains ten identical light chains

A

IgM - pentamer

50
Q

each molecule of Ig__ contains 4 identical antigen binding sites

A

IgA

51
Q

what antibody class is found most abundant in breast milk?

A

IgA - found in secretions

52
Q

what are the steps of ELISA assay? (what is specifically added when)

A
  1. coat wells with ANTIGEN OF INTEREST
  2. add PATIENT SERUM
  3. add anti-human Ab
53
Q

Ig___ binds intact antigen

A

IgM

54
Q

FcR for IgG:
a. binds intact antigen
b. transduces signal in T-cell antigen receptor complex
c. aids phagocytosis

A

c. aids phagocytosis - phagocytes have receptors for Fc of antibodies

Foundations Exam 2 (42 decks)

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