Brainscape's Knowledge GenomeTM

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


See full index

Microimm 2500 > (I) Lecture 8: B cell Immunity Part I > Flashcards

(I) Lecture 8: B cell Immunity Part I Flashcards

1
Q

B cells roles

A
  • production of antibodies
  • control of extracellular pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are B cells developed?

A

In adult bone marrow
- bone marrow has many niches filled w/ hematopoietic cells

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

B cell development

A

During development, BCR genes in variable region are rearranged (DNA RECOMBINATION)
- why each B cell has a UNIQUE specificity against a unique antigen

NEGATIVE SELECTION: Those receptors who recognize self antigens get eliminated before leaving bone marrow
- so B cells don’t attack good cells

Naive B cells then enter circulation (with BOTH IgM and IgD)

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

Immature vs Mature B cell

A

immature B cell has only IgM

mature B cells has both IgD and IgM initially with the SAME SPECIFICITY

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

B cell activation

A

Contact w/ antigen in SLT activates B cells and leads to clonal expansion

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

Plasma cells

A

effector B cells
- make and secrete antibodies (IgM first)
- also make memory B cells

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

Antigen recognition

A

Shape and size of antigen determines specificity of recognition by antigen binding site of receptor

antibodies can recognize linear (exposed) or conformational determinants in folded proteins

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

BCR and antibody

A

BCR: membrane-bound form (surface of naive and memory B cells)

Antibody: secreted form (BCR secreted by plasma cells)

BOTH have the same antigen specificity
BOTH can bind pathogen/antigen directly (unlike TCR)
BOTH can bind to protein and non-protein antigens (unlike TCR)

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

Immunoglobulin classes

A

5 types
- IgM, IgD, IgG, IgE, IgA

Difference is in heavy chain CONSTANT REGION

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

Types of antigens that bind to BCRs

A

extracellular pathogens and toxins/allergens

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

Non-protein antigens

A

Multiple identical epitopes (ex. polysaccharides)
- B cells can bind but T cells cannot
- response does not involve T cells

NO long-term protection = NO high affinity antibodies

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

Locations of B-cell development and activation

A

Bone marrow
- generation of BCRs
- negative selection

SLT
- migration of B cells through circ system to lymphoid organs and B-cell activation
- antibody secretion + memory cells

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

B cell activation steps

A

Antigen recognition by follicular T cells induces signals that activate B cells
1. BCR binds to antigen
2. B cell and T cell bind (Co-stimulatory signaling)
3. Cytokine signaling

AFTER these 3 steps:
- clonal expansion: B-cell proliferates
- differentiation: plasma called, germinal centre B cells and memory B cells

activation happes in SLT

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

What happens if B cells don’t encounter its antigen? If they do?

A

If B cells do not encounter their antigen, it remains inactive and recirculates

If B cells bind its antigen it is activated

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

Where does B cell activation happen?

A

In the SLT

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

Germinal centre

A
  • made up of rapidly dividing B-cells, follicular dendritic cells, T follicular cells (T cells are about 10%)
  • largest 7-12 days after antigen stimulation
  • where somatic hypermutation and class switching of antibodies happens
17
Q

Where so somatic hypermutation and class switching of antibodies happen?

A

In germinal centres

18
Q

How are germinal centres formed?

A

Activated B cells form germinal centres

  1. Naive B cells from bone marrow travel to lymph node and leave via efferent lymph
  2. If B cells encounter its antigen, they form a primary focus and start proliferating into a germinal centre
  3. Plasma cells generated during proliferation exit the lymph node
19
Q

Does T cell or B cell immunity happen first?

A

T cell immunity happens first (T cells are needed for B cells to get activated

20
Q

Paths of a naive B cell

A

If there are NO T cells, a naive B cell becomes a short-lived plasma cell w/ IgM

If there are T cells, a naive B cell enters the germinal centre (with Tfh) where it can differentiate to:
- long-lived class-switched plasma cell (w/ surface IgG or IgA) with improved affinity due to class switching and somatic hypermutations
OR
- long-lived memory B cell

21
Q

First immunoglobulin molecule made

A

Mature B cells produce IgM first

Can produce other Ig classes via CLASS SWITCHING

22
Q

Affinity maturation

A

B cells in the germinal centre can undergo somatic hypermutations in which the variable region of Ig genes are changed to improve affinity to specific antigen

23
Q

Somatic hypermutation

A

Mutations in the heavy-chain and light-chain of VARIABLE region

IN germinal centre

improves affinity for antigen BUT does NOT change specificity

24
Q

Class switch

A

Heavy-chain CONSTANT regions are replaced by the heavy-chain constant region of another isotype

Different cytokines will activate class switching for different Igs

25
Q

Functions of antibodies

A
  • neutralization of pathogens and toxins
  • opsonization
  • complement activation (lysis, improvement of phagocytosis)
26
Q

Functions of antibodies

Neutralization

A

Prevents toxins/viral particles from interacting w/ cells

Antigen protects cell by blocking binding of toxin

27
Q

Functions of antibodies

Opsonization

A

Coating fo microorganisms w/ antibodies and complement proteins to ENHANCE PHAGOCYTOSIS

  1. PRR binds to PAMP
  2. CR I receptor binds to C3b
  3. Fc receptor binds antibody = formation of pseudopos to engulf pathogen
  4. Phagosome formation
28
Q

Functions of antibodies

Complement activation

A

Bound antibodies form a platform that activates the 1st protein in complement system = deposit complement protein that form MAC on surface of bacteria

  • also help w/ inflammation + immune cell recruitment; cell lysis and activation
29
Q

Fc receptors

A
  • family of cell-surface molecules that bind to Fc portion of immunoglobulins
  • phagocytes express Fc receptors
  • helps recognize and phagocytose opsonized pathogens
  1. bacterium is coated w/ complement and IgG
  2. C3b binds to CR1 and antibody binds to Fc receptor = bacteria is phagocytosed
  3. macrophage membrane fuses = phagosome
  4. lysosome fuses with vesicles and degrades bacteria
30
Q

Compatibility of Blood Transfusion

A

The problem with blood transfusion is the antibodies your body makes against antigens of transfused blood

Incompatible blood transfusion results in antibody-mediated phagocytosis of donor RBCs

ex. type A blood can’t receive type B blood b/c it makes anti-B antibodies

31
Q

What would this scenario mean?

No serum IgM, IgG or IgA

A

NO B cells are produced

32
Q

Agammaglobulinemia

A
  • mostly seen in males and inherited from mother
  • first 10 months of life are good (b/c they get antibodies from mother)
  • frequent BACTERIAL infections (innate immunity and T cells are okay to kill viral infections)
  • no B cells produced (no serum IgM, IgG or IgA)
  • treated w/ IVIG

Microimm 2500 (29 decks)

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