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Module 3 > Overview of Adaptive Immunity > Flashcards

Overview of Adaptive Immunity Flashcards

1
Q

Name the 5 routes of infection

A
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2
Q

Recall the 4 stages of an immune response

A
  1. Recognition
  2. Recruitment
  3. Elimination
  4. Resolution and repair
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3
Q

Briefly outline how the innate and adpative immune system are linked

A

INNATE (Day 1-3)

  1. Pathogen infects cells
  2. Cells release alarmins
  3. Alarmins recognised by PRRs
  4. Release of cytokines and chemokines
  5. Innate effector cells kill infected cells

DENDRITIC CELLS (Day 4-7)

  1. Antigens are released from cells and APCs recognise them
  2. APC presents to CD4+ cells

ACQUIRED (Day 7-9)

  1. Activate CD8+ and B cells
  2. Clear infected cells
  3. Antibody production
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4
Q

Which cells are involved in the adaptive immune system

A

Dendritic Cells

T cells

B cells

Innate cells kill infected cells, Adaptive cells highly specific and target signel strains of bacteria

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5
Q

Define adaptive immunity

A

Immune response:

  1. Mediated by T and B cells
  2. Highly specific and focused
  3. Has memory
  4. Needs time
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6
Q

Which genes code for MHC and how many of these genes are there?

A

HLA genes

6 genes

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7
Q

What are the principles of adaptive immune defence (3)

A
  1. Recognition of self vs non-self
  2. Licensing of immune response
  3. Communication between cells

Clonal Selection, Cell migration

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8
Q

How does the immune system recognise self vs non-self

A
  1. Use of PRRs (to recognise PAMPs/DAMPs)
  2. MHC

MHC - Major Histocompatibility Complex

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9
Q

Define tolerance and describe it’s subtypes

A

Tolerance: State of unresponsiveness (to substances that can induce immune response)

  1. Central: destroy self-reactive T/B cells before they enter circulation
  2. Peripheral: destroy self-reactive T/B cells in the circulation
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10
Q

Explain the process of clonal selection (4)

A
  1. Lymphocytes have a single unique receptor
  2. Clonal deletion to remove self-reactive lymphocytes
  3. Antigen activates receptor
  4. Proliferation and differentiation of activated lymphocyte
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11
Q

An immune response needs to be licensed and this is done through 3 signals in T cells

A
  1. Antigen recognition (TCR-MHCII)
  2. Co-ctimulation (CD28-CD80)
  3. Cytokine stimulation
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12
Q

Explain how cells move from blood to tissue with receptors invovled (5 steps)

A
  1. Tethering
  2. Rolling (selectin)
  3. Adhesion triggering (integrin)
  4. Extravasation
  5. Chemotaxis
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13
Q

Outline receptors and ligands involved in cell comomunication between APC and T cell

A
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14
Q

Define an antigen and the epitope

A

Antigen: Proteins or molecules that can induce an adaptive immune response

Epitope: the region where receptors/antibodies bind on an antigen

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15
Q

Outline the function of a dendritic cell

A

Dendritic cells activated by PRRs (innate)

Capture antigens

Travel to lymhpoid tissue via lymphatic system where they mature

Present antigen to lymphocytes (T cell)

Specialised APC which patrol tissues - main function is surveillance

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16
Q

Complete the table on MHC/TCR interaction

A
17
Q

Where do T and B cells mature?

Differentiate between the two T cell subtypes

A

T cell: thymus

B cell: bone marrow

Th (helper) = CD4+, recognises MHCII

CTL (killer) = CD8+, recognises MHCI

TCR=CD3

18
Q

Explain how cytotoxic T cells induce apoptosis of target cells (2)

Apoptosis = programmed cell death, characterised by fragmentation of DNA and no inflammation

A

CTL induce apoptosis in two ways:

Granule Exocytosis

  1. Granule containing perforin and granzyme
  2. Perforin creates pores on target cell membrane
  3. Granzymes enter and induce apoptosis via caspase cascade

Fas Pathway

  1. T cell Fas Ligand binds to target cell Fas
  2. FADD and initiator caspase activate caspase cascade
  3. Apoptosis
19
Q

How do T and B cell receptors recognise pathogens/non-host protein structures

A

T cells: primary structure (linear aa)

B cells: tertiary structure (epitopes)

20
Q

Describe the effect of HLA-B57+ in a patient with HIV and describe what happens when the same virus is transmitted to a patient with HLA-B57-

A

HLA-B57+ presents epitope of ?reverse transciptase

Virus degrades RT and therefore decreases its fitness (i.e. HLA-B57 protective against HIV)

Transmission to HLA-B57- reverts the virus back to its fitter self -> increase virus activity

21
Q

Name the 5 T helper cell subsets

A
  1. Th1
  2. Th2
  3. T17
  4. Treg
  5. Tfh
22
Q

What cytokines do Th1 cells produce and what is its function

A

IFN-γ

Intracellular immune response

23
Q

What cytokines do Th2 cells produce and what is its function

A

IL-4. IL-5, IL-13

anti-multicellular organism (involved in allergy)

24
Q

What cytokines do Th17 cells produce and what is its function

A

IL-17, IL-22

Autoimmune (arthritis IL-17)

Bacterial control

25
Q

What cytokines do Treg cells produce and what is its function

A

IL-10, TGF-β, IL-35

Immunosuppressive (regulates T cell activity)

26
Q

What cytokines do Tfh cells produce and what is its function

A

IL-21

Reside in B cell follicles - generation of isotype-switched antibodies

27
Q

B-cells make antibodies which are found on their surface (BCR). We need a large pool of antibody diversity to be able to respond to pathogens. We can make 1010 antibodies but don’t have 25,000 genes to code for all of these. How is diversity generated?

A

Diversity generated through Immunoglobulin Gene Rearrangment

There is rearrangment of vairable (V), joining (J) and sometimes diversity (D) segments to form the diverse antibody pool.

28
Q

Describe the 3 steps that occur in B cells after antigen exposure

A
  1. Antibody production
  2. Affinity Maturation
  3. Memory
29
Q

Explain what affinity maturation i in B cell fuction

A

The process where B cells produce antibodies with higher affinity to antigen after many antigen presentation. Regulated by Tfh cells with IL-21

30
Q

Explain the T/B cell interaction in B cell activation

A
  1. Ag presented to B cell by T cell or internalised and processed MHCII -> SIGNAL 1
  2. CD4+ T cell recognise Ag with co-stimulation from CD28-B7
  3. Leads to increased CD40L expression which binds to CD40 on B cell -> SIGNAL 2
  4. T cell cytokines bind to B cell receptors -> SIGNAL 3
  5. B cells proliferate and differentiate
31
Q

Describe the structure of an antibody

A

Variable region

Constant region

4 chains (2 heavy, 2 light)

32
Q

Describe the 3 main functions of antibodies

A
  1. Neutralisation
  2. Opsonisation
  3. Coomplement activation
33
Q

Define memory T/B cells and their effect in pathogen exposure

A

Cells that become quiescent instead of effector cells

Re-infection causes larger response at a faster rate and requires less stringent activation

34
Q

Which lymphocyte goes through isotype switching and affinity maturation - T or B cells

A

B cells

T cells do NOT isotype switch or have affinity maturation

35
Q

Briefly outline the typical life of a memory t cell from naivity

A

Naive T cell

Expansion of effector cell

Contraction of memory cell

Secondary expansion from memory cell is massive and faster

36
Q

Explain T cell exhaustion

A

Chronic inflammation leads to decreased function of effector cells.

They stop releaseing IFN-γ and IL-2

Start expressing anti-proliferative receptors such as PD-1 (binds to PDL in cancer cells)

37
Q

Describe how the immune response (memory) can go wrong

A

Immunopathology (excess activity)

Autoimmunity

Allergy

Module 3 (17 decks)

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