Brainscape's Knowledge GenomeTM

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


See full index

Immunity > B Cell/Antibody Function > Flashcards

B Cell/Antibody Function Flashcards

1
Q

X-linked Agammaglobulinemia (XLA)

A

Defect in gene encoding Bruton’s tyrosine kinase (BTK)

Defective enzyme function
Defective enzyme level
Responsible for B cell maturation, survival, proliferation
X chromosome

Absence of B cells
Decreased IgG, IgA, IgM

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

Immune Deficiency (primary, secondary causes, estimations, live births)

A

Primary: Not caused by other factors; you’re born with it or develops for unclear reasons

Secondary: Caused by other factors
Diseases, medications, malnutrition could cause immune deficiency

200 primary immune deficiency diseases
1:1,200 live births

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

B cell deficiencies (what is absent, reduced, what is infectious consequence)

A

Absent or reduced follicles in germinal centers in lymphoid organs

Reduced serum Ig levels

Infectious consequence:
Pyogenic bacterial infections, enteric bacterial and viral infections

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

T cell deficiencies (reduced or defective, infectious)

A

May be reduced T cell zones in lymphoid organs

Reduced DTH reactions to common antigens

Defective T cell proliferative responses to mitogens in vitro

Infectious:
Viral and other intracellular microbial infections (Pneumoncystis jiroveci, other fungi, non-TB mycobacteria)

Virus associated malignancies
(EBV lymphomas)

Bad bacteria, opportunistic infections

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

Innate immune deficiencies

A

Variable abnormalities, depending on which component

Variable infections: pyogenic, bacterial, viral

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

B Cell maturation (and CD surface molecules)

A 
Hematopoietic stem cell
Lymphocyte Precursor
Pro-B cell
~VDJ recombination~
Pre-B cell
BTK checkpoint
Immature B cell
mature B cell

Surface molecules aka CD20 CD19 etc. change throughout development. If you want to give a drug that targets CD20, it would wipe out ever cell that has that marker, but not all (ex. plasma protein)

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

B lymphocyte (antigen recognition, effector functions)

A

Recognizes antigen
Neutralizes microbe
Phagocytosis
Complement activation

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

Helper T lymphocyte (antigen recognition, effector functions)

A

Microbial antigen presented by APC
Releases cytokines

  1. Activation of macrophages
  2. Inflammation
  3. Activation (proliferation and differentiation) of T and B lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cytotoxic T lymphocyte

A

Infected cell expressing microbial antigen

Killing of infected cell

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

B lymphocyte function (3)

A
  1. Produce antibodies
    T dependent or T independent
    Membrane bound (B cell receptor)
    Secreted
  2. Plasma cells: Long living mature B cells
    Produce high affinity antibodies even after antigen removal
    Stimulated by infections and vaccines
  3. Memory cells: long living mature B cells
    Do not produce antibody
    Ready to rapidly respond upon antigen reintroduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Antibody structure

A

2 identical heavy chains (Y) (1V, 3-4C domains)
2 light L chains (1V, 1C domain)

Variable V region
Variable
Diversity
Joining

Constant C region

Disulfide bonds

C terminus either anchored in plasma membrane (BCR) or terminate so it is secreted

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

Immunoglobulin domain (antibody)

A

Folded layers of a B pleated sheet held together by a disulfide bond connected by protruding loops

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

Fab (antibody)

A

Fragment antigen binding region

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

Hinge region (antibody)

A

flexibility for increased binding to the 2 Fab regions

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

Fc (antibody)

A

Fragment crystalline region

Crystalizes in solution

Responsible for the biologic activity of antibodies

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

Complementarity determining region (CDR) loops

A

In V regions of immunoglobulin domain (Vh and Vl chains)
3 on each

Responsible for antigen recognition
Single antigen that it can recognize
High affinity
CDR3 has the greatest variability and contributes the most to antigen binding

Light chain types: K and g
No functional difference

17
Q

IgA

A

IgA1,2

3.5mg/mL serum

6 day half life

Mainly dimer, also monomer, trimer

Mucosal immunity (transport of IgA through epithelia)
Major isotype in mucosal lymphoid tissues via TGF-B
18
Q

IgD

A

Trace serum

3 day half life

Monomer

Naive B cell antigen receptor

19
Q

IgE

A

0.05 mg/mL serum concentration

2 day half life

Monomer

Defense against helminthic parasites
Mast cell degranulation (Immediate hypersensitivity)
Allergic response

20
Q

IgG

A

IG1-4

13.5 serum concentration

23 day half life

Monomer

  • Fc receptor dependent phagocyte responses
  • Opsonization
  • Complement activation
  • Antibody dependent cell-mediated cytotoxicity
  • Neonatal immunity (can pass placenta; how newborns have immunity; their own immunity develops 4-6mo later)
  • Feedback inhibition of B cells
  • Memory antibody produced in response to vaccination and infection offering LT protection post exposure

most abundant Ab in the plasma

21
Q

IgM

A

1.5 mg/mL serum

5 day half life

Pentamer

Naive B cell antigen receptor (monomeric form)

Complement activation

Produced rapidly after vaccination but degrades rapidly and doesn’t offer long term protection

22
Q

Binding region of antibody (what type of interaction? affinity? avidity? cross-rxn?)

A

Vh and Vl chain CDRs
Form clefts where epitope of molecules bind
Epitopes may be AA (linear) or shape related (conformational)

Reversible, non-covalent interactions
H bonding
Hydrophobic
Charged based

Affinity: strength of one Ag-Ab bond
Increases with repeated exposure (why we repeat vaccination)

Avidity: total strength of multiple bonds

Cross reactivity: Abs may bind other structurally related Ags with similar epitopes

23
Q

T-dependent B cell Responses

A

APCs present to T cells that activate B cells to induce class switching and affinity maturation

Called:
Isotype-switched high affinity antibodies
Memory B cells, long-lived plasma cells

T cell helps B cell produce antibodies long term

Otherwise, PROTEIN antigens cause weak or absent antibody responses without T cell help

24
Q

T-independent B cell responses

A

Polysaccharides, lipids, other non-protein antigens elicit antibody production without involvement of T cells

Simple process to T dependent antigens
Less isotype switching
Less affinity maturation

Mainly IgM, low-affinity antibodies, short-lived plasma cells

25
Q

Common Variable Immune Deficiency

A

Recurrent bacterial sinopulmonary infections, GI infections, systemic complications

Because you don’t make antibody

Low IgG <400
Low IgA and/or low IgM

Insufficient responses to vaccinations

Unknown and likely multiple etiologies

Onset at any age

26
Q

BCR Signaling (B cells and TLRs)

A

B cells express complement receptor for activation when exposed to microbial antigen

  1. Microbial bound C3d (released from C3 during complement activation) binds to complement receptor 2 (CR2) on the B cell surface to activate B cells
  2. C3d-CR2 binding enhances B cell activation as part of the innate immune response

TLR activates B cells by promoting B cell proliferation, differentiation, and antibody secretion

example of adaptive + innate immunity working together

27
Q

BCR Signaling - mechanism

A
  1. Ab bound to antigen
  2. Tyrosine phosphorylation occurs
  3. Activation of downstream enzymes via biochemical intermediates
  4. Production of transcription factors leading to the immune response
    (Myc, NFAT, NFkB, AP-1)
28
Q

What happens when an antigen is recognized by both the T and B cell?

A
  1. Naive T cell activated by Ag presented by DCs differentiates into Th cell
  2. Naive B cell activated by Ag binding

Migrate toward each other to cause the antibody response

Some migrate back to form germinal centers producing further antibody response

29
Q

What interaction must occur to allow B cells to produce other isotypes?

A

Th cells express CD40L that binds to CD40 on the B cell

Binding must happen in order to get isotype switching

(B cells normally just make IgM/IgD)
In order to make IgG, IgA, and IgE, this interaction must occur with cytokine mediators

> > > B cell differentiation and proliferation

30
Q

Isotype switching (VDJ)

A

VDJ exon encoding the V domain of an IgM heavy chain and moves it adjacent to a downstream C region

Activation-induced deaminase (AID) removes uracil to create DNA nicks (induced by CD40)

dsDNA breaks into 2 switch regions and brought back together and repaired (removal of a portion of DNA)

New heavy chain isotype (IgA, G, E)
same specificity as before

31
Q

Isotype switching (cytokine dependent)

A

IL-10 from Tfh cells stimulate isotype switching to IgG via IFN-g
>opsonizes microbes
>promotes microbial phagocytosis and intracellular killing

IL-4 from Tfh cells stimulate isotype switching to IgE
>response to helminthic infections with IL-5 stimulated eosinophils
>generate the allergic response

32
Q

Affinity maturation

A

Affinity of antibodies changes with prolonged or repeated Ag exposures

Th cell-dependent protein antigens
Somatic hypermutation of immunoglobulin genes
Selection of high-affinity B cell survival (others will die)

33
Q

Hyper IgM Syndrome

A

X linked
Defective CD40-CD40L binding due to defective CD40L gene

Autosomal recessive form associated with defect in AID

IgM is elevated
IgG and IgA (helpful for fighting infections) is absent due to absence of class switching
Normal B cell numbers

34
Q

Selective IgA Deficiency

A

IgA is the secretory antibody
Located on mucosal surfaces
Prone to sinopulmonary bacterial infections, otitis, and conjunctivitis
Prone to GI infections
Prone to allergies and autoimmune disease

35
Q

Monoclonal Antibodies

A
  1. Isolate spleen cells from mouse immunized with antigen X
  2. Fuse spleen cells (that produce x-antibody) with mutant immortal myeloma line (unable to grow in selection medium
  3. Only fused cells (hybridomas) grow
  4. Screen supernatants of each clone for anti-x antibody and expand positive clones

Hybridomas producing monoclonal anti-X antibody

Select antibody of desired specificity for targeted therapy for disease

36
Q

IgG supplementation Therapy

A

Pooled from plasma donors (from people who have been sick or vaccinated)
Intravenous or subcutaneous infusions
Given on a weekly to monthly basis for whole life
Does not work in patients who have selective IgA deficiency

Give to people who don’t make enough IgG to replenish immune system

37
Q

CD19, CD20, CD21

A

A surface marker on B cells

Immunity (3 decks)

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