S7 Adaptive Immune System Part 2 Flashcards

1
Q

When do antigen presenting cells mature?

A

When they ‘capture’ an antigen

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2
Q

Where in lymphoid tissue do T cells become activated, B cells become activated and where do they meet?

A
  • parafollicular cortex (T cell zone)
  • lymphoid follicle (B cell zone)
  • edge of follicle
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3
Q

Where are B and T lymphocytes produced? Where do they mature?

A

Produced in bone marrow

T cells - mature in thymus
B cells - mature in tissues following contact with the antigen

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4
Q

Where do B and T lymphocytes accumulate?

A

In lymphoid tissues e.g. MALT, lymph nodes and spleen

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5
Q

What are the main 3 lymph nodes?

A
  • cervical (neck)
  • axillary (armpit)
  • spleen (inguinal)
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6
Q

What is lymphadenopathy?

A

Swelling that occurs in lymph nodes/tissues/etc when B and T cells are activated by the antigen and start proliferating

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7
Q

How are antigens recognised by T lymphocytes?

A

Antigens are recognised by T cell receptors (TCR)

  • CD4+ T cells recognise peptides presented by MHC class II molecules
  • CD8+ T cells recognise peptides presented by MHC class I molecules
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8
Q

What is a T cell receptor (TCR) like?

A
  • alpha and beta chains (variable region)
  • CD3 complex
  • accessory molecules - CD4 or CD8
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9
Q

How are T lymphocytes activated?

A

By co-stimulation

* a co-stimulatory protein is needed to fully activate a T cell

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10
Q

What activates CD4+ T cells to produce the different variants?

A

Activated by chemical mediator e.g. IL-12/4/1/6/10 or TGF-beta

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11
Q

What do TH1 CD4+ T cells cause stimulated by IL-12?

A
  • CD8+ T cells to differentiate
  • macrophage recruitment and activation
  • stimulates B cells to produce IgG or IgA

This is cell mediated immunity (against extracellular pathogens - bacteria, viruses, fungi)

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12
Q

What do TH2 CD4+ T cells cause stimulated by IL-4?

A
  • stimulate B cells to produce IgE
  • activate eosinophils to kill pathogens
  • activates mast cells against allergies

This is humoral immunity (against extracellular pathogens - parasites, worms)

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13
Q

What do TH17 CD4+ T cells cause stimulated by IL-1/6?

A
  • recruitment and activation of neutrophils
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14
Q

What do THreg CD4+ T cells cause stimulated by IL-10/TGF-beta?

A
  • tolerance

* immune suppression

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15
Q

What is required to activate effector CD8+ T cells?

A

TH1 (for activation of effector CD8+ T cells from naive CD8+ T cells)

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16
Q

If an unaffected cell has MHC I molecules presenting self-antigens will this be detected by cytotoxic lymphocytes?

A

No

17
Q

How are antigens recognised by B lymphocytes?

A

By B cell receptors (BCR) which are membrane bound antibodies and are unique and specific for each cell

18
Q

What types of antigen to B lymphocytes recognise?

A
  • macromolecules (proteins, polysaccharides, lipids, nucleic acids)
  • small chemicals
19
Q

What is required for activation of B lymphocytes?

A

Multiple signals

  1. BCR engagement - signal transduction
  2. TCR engagement - this is antigen specific
  3. Cytokine release
20
Q

Why do you need T helper cells involved in B lymphocyte activation?

A

If didn’t have T helper cells, would only be able to produce IgM antibodies, T helper cells are involved in the switching of antibody production to e.g. IgG due to the CD40L on T cells

21
Q

Production of which antibodies is thymus-dependent?

A

IgG, IgE and IgA

22
Q

Why do we have booster vaccinations?

A

To increase the amount of IgG (better protection than IgM) - in secondary response

23
Q

How can you tell if exposure to an infection is acute of chronic?

A

By the type of antibody present

  • acute - more IgM
  • chronic - more IgG
24
Q

What is the role of antibody IgA?

A

Involved in mucosal immunity e.g. GI tract and respiratory tract immunity

25
Q

What is the role of antibody IgM?

A

Complement antibody

This is the first antibody produced

26
Q

What is the role of antibody IgE?

A

Immunity against helminths and allergies

27
Q

What should you consider/assess when looking for signs of an adaptive immune response?

A
  • portal of entry
  • is there a fever?
  • any acute phase reactions e.g. CRP
  • neutrophil number?
  • phagocyte function?
  • lymphadenopathy
  • lymphocyte number and function serology
28
Q

What medical achievements have been derived from studying the adaptive immune response?

A
  • disease prevention - vaccines
  • immunoglobulin therapies for those with immune deficiencies
  • immediate protection - antibody transfer (passive immunisation) e.g. for rabies
  • diagnostic tests (antibody based) - for infectious diseases, autoimmune diseases and blood type and HLA types
29
Q

DiGeorge syndrome is an immune deficiency resulting from an impaired thymic development. Which immune components will be affected in these patients?

A

T cell and B cell function

Need T cells to fully activate B cells

30
Q

What is the type of CD4+ T cells that respond to intracellular pathogens by recruiting and activating phagocytic cells?

A

TH1

31
Q

If a patient doesn’t have CD40L on their T cells (due to a mutation), what antibody will they most likely produce in response to Staphylococcus aureus?

A

IgM

32
Q

Which MHC molecule expresses the viral peptides of varicella zoster virus?

A

MHC I

33
Q

How would you check if someone has had chickenpox before?

A

Serology for varicella zoster virus antibodies (IgG)

34
Q

Which factors from the adaptive immunity will be used against the virus?

A

CD8+ T cells (cytotoxic T cells)

Activated by TH1 cells