Lymphocytes Flashcards

1
Q

Why do we need adaptive immunity?

A

Protect us from repeat infections with same pathogens

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2
Q

What does the adaptive immunity do?

A

Improve the efficacy of the innate immune response

Focuses a response on the site of infection and the organism responsible

Has memory

Needs time to develop

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3
Q

When does the immune system exhibit memory?

A

Once the immune system has recognised and responded to an antigen

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4
Q

What cells are involved in the ‘cell-mediated’ response?

A

T cells

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5
Q

What cells are involved in the ‘humoral’ response?

A

B cells

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6
Q

What are the two roles of T cells?

A

Production of cytokines to help shape immune response —> CD4 (helper)

Kill infected cells —> CD8 (killer)

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7
Q

What is the role of B cells?

A

Produce antibody

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8
Q

How do T and B cells recognise pathogens?

A

T cell and B cells receptors that detect antigens

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9
Q

What are epitopes?

A

Region of an antigen which the receptor binds to

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10
Q

What type of epitope do T cells recognise?

A

Linear epitopes in context of MHC molecules
—> primary structure if antigen

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11
Q

What type of epitope do B cells recognise?

A

Structural epitopes —> 3D structure of the antigen in space
—> tertiary structures of antigen

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12
Q

What is clinal expansion?

A

Each lymphocyte bears single unique receptor
—> interaction between foreign molecule and receptors leads to activation and clonal expansion

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13
Q

What is the problem of antigen diversity?

A

We need a massive repertoire of lymphocyte receptors to deal with antigen diversity

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14
Q

How is the antigen receptor diversity solved?

A

Through genetic recombination

Each BCR receptor chain is encoded by separate multi gene families on different chromosomes

During B cell maturation these genes segments are rearranged and brought together

—> called Immunoglobulin gene rearrangement

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15
Q

What is the Major Histocompastabilty complex?

A

Plays a central role in defining self and non self

Present antigens to T cells

Critical in surgery and donor matching

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16
Q

What are the two types of MHCs?

A

MHC class I

MHC class II

17
Q

What are MHC I made of?

A

All nucleated cells —> although at various levels

Single variable alpha chain plus common microglobulin

18
Q

What are MHC II made of?

A

Normally only on professional APCs

Have 2 chains —> alpha and beta

19
Q

What is MHC encoded by?

A

HLA genes in humans

Polygenic —> 3 class I and 3 class II loci

Expression is codominant

Each person can have up to 6 of each gene if completely heterozygous

20
Q

How do MHC and TCR interact?

A

Present intracellular pathogens/antigens to:

MHC I to CD8 T cell TCRs

MHC II to CD4 T cell TCRs

21
Q

What are the two families of T cells?

A

CD4 helper T cell

CD8 killer T cell

22
Q

What do CD4 cells do?

A

Produce cytokines —> which have diverse actions on a wide range of cells + influence outcome of the immune response

23
Q

What do CD8 cells do?

A

Kill targets by programmed cell death (apoptosis)

CTL store perforin —> release after target recognition —> perforin molecules polymerise, from pores

24
Q

How do CD8 cells kill infected cells?

A
  1. CD8 cell scans cells, looks for non-self MHC
  2. Virus infects the cell and release its contents
  3. Cell starts making viral proteins
  4. Displays these as non-self MHC
  5. CD8 cells detects non-self MHC and attacks
  6. CD8 kills the virally infected cell
25
Q

What is the structure of antibodies?

A

2 heavy and 2 light chains
—> divided into 2 areas —> constant and variable region

Variable region has a huge potential for diversity

26
Q

What are the 3 main functions of antibodies?

A

Neutralisation

Opsonisation

Complement activation

27
Q

What happens during neutralisation?

A

Antibody binds to active site on virus/bacteria ad prevents them from functioning

28
Q

What happens during opsonisation?

A

Antibody makes a pathogen more attractive for phagocytosis

29
Q

What happens during complement activation?

A

Cascade of events driven by antibody which leads to death of the bound pathogen

30
Q

What are the 5 main antibody classes?

A

IgG —> highest opsonisation and neutralisation activities

IgM —> produced first upon antigen invasion, increases transiently

IgA —> expressed in mucosal tissue, forms dimmers after secretion

IgD

IgE —> allergy

31
Q

Where do B cells come from?

A

Derived from HSC in bone marrow

Migrated into circulation and into lymphoid tissues

Mature B cells are specific for particular antigen

32
Q

How is the activation of B cells regulated?

A

Naive B cells require accessory signal:
—> directly from microbial constituents (thymus independent)
—> from a T helper cell (thymus dependent)

33
Q

What is the thymus independent path?

A

Microbial constituents

  • directly activate B cells w/out help of T cells

Makes only IgM and no memory

34
Q

What is the thymus dependent path?

A

T helper cells

1) The membrane bound BCR recognises antigen

2) The receptor-bound antigen is internalised and degraded into peptides

3) Peptides associate with ‘self’ molecules (MHC II) and is expressed at cell surface

4) This complex is recognised by matched CD4 T helper cell (that has been activated by recognising an antigen presented via MHC II by an APC like a dendritic cell)

5) B cell activated by co-stimulation markers and cytokines that Tfh release

  • all Ig classes and memory