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Immunology > Autoimmune diseases, transplantation and AIDS > Flashcards

Autoimmune diseases, transplantation and AIDS Flashcards

1
Q

What are the two classifications of autoimmune diseases?

A
  1. Based on whether one tissue or multiple tissues are affected.
  2. Distribution of auto antigens involved in response i.e organ specific, organ non-specific.
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2
Q

Give an example of primary and secondary autoimmune disease pathology.

A

Hashimoto’s thyroiditis:
primary- destruction of thyroid tissue
secondary- hypothyroidism due to loss of thyroid.

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3
Q

What are the mechanisms of auto-antibody mediated immune pathology and give examples?

A

Damage or destruction

  • complement mediated lysis: haemolytic anaemia
  • opsonisation and phagocytic removal: thrombocytopenia

Alteration of function

  • stimulation of receptors: Graves disease
  • inhibition of function: Myasthenia gravis
  • blockage of function: pernicious anaemia

Deposition of immune complexes- initiate inflammatory reaction: systemic lupus erythematosus (SLE)

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4
Q

What is concordance?

A

Incidence of disease in related individuals which provides evidence of genetic/ environmental basis of disease.

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5
Q

Possible environmental influence of autoimmune disease

A
  • Microbial agents
  • Drugs
  • Toxins- UV, pesticides, pollutants, smoking
  • Diet
  • Hygiene
  • Vitamin D- may suppress Th17 development
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6
Q

Are autoimmune diseases multigenic and why?

A

Yes because many genes are polymorphic which can mean that different forms of the protein are made and people can have altered protein activity or protein levels.

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7
Q

What are the main susceptibility genes?

A

MHC

Non-MHC: CTLA-4, sex related genes

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8
Q

How can drugs cause an autoimmune reaction?

A

The drug binds to a self-antigen, modifies it and creates a T-cell epitope that appears foreign so it’s attacked.

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9
Q

What is chronic autoimmune disease and how does it develop?

A
  • Inability to clear self antigen
  • Develop via positive feedback from inflammation.
  • Broadening of autoimmune response- epitope spreading as hidden.
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10
Q

What is the definition of transplantation?

A

The artificial transfer of tissue, cells or organs, from one anatomical site to another to replace lost or failing function

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11
Q

What are the rejection kinetics in transplantation.

A

If you give a graft, it’s rejected. If you give another graft from the same person then it’s rejected even quicker.

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12
Q

What are the current ongoing challenges in transplantation?

A
  • Managing organ rejection: long term immune suppression and chronic rejection
  • Organ supply
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13
Q

What are the most routinely performed transplants?

A

Kidney, liver, heart, pancreas, lung, intestine, cornea

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14
Q

What are the 4 types of grafts and who are they from?

A

Autograft: from yourself
Isograft: from your identical twin
Allograft: from a stranger
Xenograft: from a different species

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15
Q

Where are the antigens for the major response encoded?

A

Mouse chromosome 17

Human chromosome 6

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16
Q

How is MHC expressed?

A

Co-dominantly

17
Q

Why does complete matching at the MHC not guarantee graft survival?

A

Still get less vigorous, slow rejection from minor histocompatibility antigens

18
Q

What are the 3 types of transplant rejection?

A

Hyperacute- occurs if the recipient has pre-existing antibody against the graft: minutes.
Acute-equivalent of primary immune response: day to weeks.
Chronic- slow, progressive loss of function: years

19
Q

Methods of preventing graft rejection.

A
  • match blood type
  • cross-match: make sure you don’t have pre existing antibodies to the donor
  • matching for HLA: the more HLA matches the more successful the transplant.
  • immunosuppression
20
Q

What is a syndrome?

A

Collection of disease symptoms with no known cause.

21
Q

Characteristics of HIV-1 and HIV-2

A

HIV-1:

  • from chimpanzees
  • more virulent
  • responsible for most AIDS infections in the world

HIV-2:

  • from sooty mangabey
  • West Africa
  • less virulent
22
Q

Structure of HIV

A
  • Retrovirus
  • dsDNA
  • Lentivirus
  • Membrane is host derived but has viral proteins which are important for attachment and entry.
23
Q

Why are host derived components advantageous for HIV?

A

Makes it camouflaged as ‘self’ so the immune system doesn’t detect and attack.
Complement cannot deposit on the membrane.

24
Q

What is advantageous about the viral spikes on HIV membrane?

A

There are only 14 of them- less targets makes it difficult to get rid off.
Structure of the spikes makes it difficult to make antibodies to.
The structure of the spikes varies in each spike.
Has a glycol shield full of sugars so it’s difficult to identify.

25
Q

What cells does HIV attack?

A

CD4 T cells
Monocytes/Macrophages
Dendritic cells

26
Q

How does HIV attach to the cell?

A

Binding causes conformational changes and reveals co-receptor such as ccr5 or cxcr4.
Binding with co-receptor causes further change and causes membrane to diffuse.
As you progress through the infection there’s a switch from R5 tropic to X4 tropic which shows the change in where the virus wants to go to (from monocyte/ macrophage/ T cells to naive T cells and DCs).

27
Q

How does HIV remain undetected?

A

The virus keeps changing so if you make a correct T cell then by the time it finds the correct virus HIV would have changes and the T cell would be incorrect again.

28
Q

Draw the HIV immunological course of infection

A

…..

29
Q

What are the 3 types of HIV patients?

A
  • Progressors-high viral set-point, progress to AIDS most quickly.
  • Viraemic Controllers- low viral set-point, progress to AIDS more slowly.
  • Elite Controllers- <1% of HIV infected people, control virus to extremely low levels, do not progress to AIDS.
30
Q

What types of anti-retroviral drugs are available?

A 
Viral protease Inhibitors			
Reverse transcriptase inhibitors
Integrase inhibitor
Fusion inhibitor
Co-receptor binding inhibitors
31
Q

What are the barriers to creating a vaccine against HIV?

A
  • Destruction by HIV of any CD4 T cell responding to a vaccine
  • Attenuated vaccine considered too ‘risky’
  • Extreme antigenic variation of HIV
  • Low immunogenicity of conserved HIV epitopes
  • Lack of animal model for AIDS
  • Lack of adequate human in vitro testing system

Immunology (11 decks)

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