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Immunology > 5. B Lymphocytes > Flashcards

5. B Lymphocytes Flashcards

1
Q

3 core protective roles of antibodies

A

Neutralisation
Opsonisation
Complement activation

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2
Q

What are leukocytes?

A

All white blood cells

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3
Q

What are lymphocytes?

A

B cells

T cells

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4
Q

Adaptive immunity

A

Improves efficacy of innate immune response
Highly targeted- Focuses a response on site of infection and organism responsible
Has memory
Needs time to develop

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5
Q

Antigen

A

Protein/ molecule that is recognised by immune system

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6
Q

Epitope

A

Region of an antigen which receptor binds to

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7
Q

What is the difference between the types of epitopes recognised by B cells and T cells?

A

T cells = linear epitopes e.g. AA sequences

B cells = structural epitopes e.g. tertiary structure

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8
Q

Which lymphocytes are involved in humoral adaptive immunity and how?

A

B Cells

Antibodies

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9
Q

Which lymphocytes are involved in cell mediated adaptive immunity and how?

A

T cells

Cytokines, killing

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10
Q

Describe B cell generation and maturation

A

Occurs in bone marrow in absence of antigen
Derived from haematopoietic stem cells
Start as progenitor B cell
Migrate into circulation and lymphoid tissue
Mature B cells are specific for a particular antigen

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11
Q

Where does specificity for an antigen reside in B cells?

A

B cell receptor (BCR)

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12
Q

Describe clonal selection

A

Each lymphocyte bears a single, unique receptor
Interaction between a foreign molecule and that receptor leads to activation
Differentiated effector cells of that lineage will bear the same receptor

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13
Q

When are self specific receptors deleted?

A

Early in development

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14
Q

Where are B cell receptors found?

A

Present in 1000s of identical copies on surface of B lymphocyte

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15
Q

Describe the structure of the BCR

A

Transmembrane protein complex composed of Ig Mu and di-sulfate linked heterodimers, Ig alpha and Ig beta.
Ig alpha and Ig beta heterodimers contain immunoglobulin-fold structure
The cytoplasmic tail of Ig Mu is too short to signal
The cytoplasmic tails of Ig alpha and Ig beta are long enough to interact with intracellular signalling molecules
Contain ITAM domains

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16
Q

How does the structure of the BCR transmit its signal into the cell?

A

Antigen binding to the BCR causes a conformational change, which drives signaling via the Ig-alpha Ig-beta heterodimer

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17
Q

What is the problem with antigen diversity?

A

Exposed to incredibly large variety of antigenic determinants
Can’t predict which will be encountered, so immune system must be able to respond to all
But - adaptive immune system is exquisitely specific
∴ need a huge pool of cells with specific receptors that can recognise huge array of antigens

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18
Q

How does the body deal with antigen diversity?

A

Encode a massive repertoire
10^10 different antibodies can be generated
Each is produced by a B lymphocyte expressing a specific BCR
25,000 genes for all functions

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19
Q

How is antigen receptor diversity generated?

A

Recombination
Each BCR receptor chain (kappa, lambda and heavy chain genes) is encoded by separate multigene families on different chromosomes
During B cell maturation these gene segments are rearranged and brought together
= Immunoglobulin gene rearrangement

20
Q

Describe the generation of variation in the light chain.

A

There are 30-40 different V and 4-5 J regions
B cell begins with germline DNA and cuts out V and J regions at random leaving only a few
Different splicing patterns give rise to more variation
VD(J) recombinase loops DNA together & chops out unwanted bit

21
Q

What is VD(J) recombinase?

A

An enzyme complex containing the proteins Rag1 and Rag2

Removes unwanted DNA

22
Q

What does deficiency of Rag genes result in?

A

SCID

As unable to do recombination

23
Q

How is generation of variation in the heavy chain different to that in the light chain?

A

Recombination of V, D and J
Constant regions functional
Constant region achieved by alternate splicing

24
Q

2 types of light chain

A

Kappa

Lambda

25
Q

What determines the class of the immunoglobulin?

A

Constant region of the heavy chain

26
Q

In what order does the gene rearrangement take place?

A

heavy chain undergoes rearrangement before the light chain

27
Q

Naïve B cell

A

Antigen specific cell that has never met its antigen

28
Q

What are the 3 key B cell pathways after antigen exposure?

A

Become plasma cells involved in antibody production
Affinity Maturation
Memory

29
Q

What is the general rule about B cell and T cell activation?

A

Need co-stimulation from an accessory signal to be activated
antigen alone is not enough

30
Q

Examples of accessory signals for naive B cells

A

Directly from microbial constituents

From a T helper cell

31
Q

What are the 2 pathways by which B cell production is achieved?

A 
Thymus dependent (T helper cell, all Ig classes, memory)
Thymus independent (microbial constituents, only IgM, no memory)
32
Q

Describe the T independent pathway.

A

often bacterial polysaccharide with a repeating subunit
Repeating unit can bind to several BCRs and drive cross-linking
2nd signal provided by microbial constituent
PAMPs such as LPS provide co-stimulation

33
Q

Describe the T dependent pathway.

A

Dendritic cells and B cells recognise, internalise and degrade antigen
B cells present the antigen on MHC Class II
Dendritic cells also present the SAME antigen on MHC Class II to a T helper cell
The T helper cell becomes activated and undergoes clonal selection
The T helper cell then moves to the lymph nodes, comes into contact with the B cell and activates it

34
Q

T-B Cell collaboration

A

Activated B cells express lympho(cyto)kine receptors
T cell derived cytokines bind to receptors on B cells
B cells proliferate and differentiate into antibody secreting plasma cells or memory cells

35
Q

Describe the process of immunoglobulin class switching.

A 
T helper cells (once bound to the B cell) can release various cytokines 
depending on the cytokine released, Ig class can be switched
36
Q

What does IL-2 allow B cells to do?

A

Proliferate

37
Q

What changes in an Ig class switch?

A

VDJ region stays the same

Cytokines lead to different exons being translated for different constant region

38
Q

What are the 3 types of B cell?

A

Naïve: No previous exposure
Effector: Plasma cell, secrete antibodies
Memory: Longer life span

39
Q

What drives the improvement of the immune response between primary and secondary exposures?

A

Somatic Hypermutation and Affinity Maturation

40
Q

Describe the process of somatic hypermutation.

A

Point mutations are induced in the VDJ regions by AID which cause slight conformational changes in the antigen-binding site.
If the change is beneficial and improves the binding between antibody and antigen then it survives
Otherwise the B cells are killed by apoptosis

41
Q

What is AID in somatic hypermutation?

A

Activation-induced deaminase enzyme
Induces point mutation in VDJ region
Swaps C to U, GC pairs become AT pairs

42
Q

Immunological memory

A

consequence of clonal selection
Antigen-specific lymphocytes (B + T) are the cellular basis
More rapid and heightened immune reaction that serves to eliminate pathogens fast
Can confer life-long immunity to many infections

43
Q

What is immunological memory the basis of?

A

Vaccines

44
Q

B cell usage

A

Major vaccine targets as induce antibody response

Monoclonal antibodies are exploited for cancer, asthma, pregnancy testing

45
Q

When do B cells become a problem?

A

Autoimmune conditions e.g. Myasthenia gravis
Allergy – IgE in anaphylaxis
Can tip into cancers (lymphomas and myelomas) especially under influence of viruses e.g. EBV

46
Q

Why is secondary response better?

A

Antibody quality improves over time (affinity maturation)

Response is rapid and heightened

Immunology (9 decks)

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