Disorders of immune system Flashcards
1
Q
Give 5 examples of things that could cause a type 1 hypersensitivity reaction
A
- Pollen
- Animal hair
- house dust mite
- moulds
- insect bites
- food - peanuts
- latex
- medicine - penicillin
2
Q
What is the process of a pollen allergy?
A
- First exposure - B cells recognise the Ag, internalise it and present to Th2 cells, which secrete IL-4, starting class-switching - B cells make IgE
- IgE produced from previous allergen exposure diffuses through body
- IgE binds to mast cells by its Fc region into mast cell Fc receptors
Second exposure to pollen
- Pollen enters and binds to the Ig, if pollen cross-links the IgE on the mast cell, it will release Histamine
- Mast cells generate other cytokines, encouraging Th cells to also produce cytokines - prolongs allergic reaction
3
Q
What causes a type II reaction?
A
Ag and Ab interaction of IgM
4
Q
Gives some examples of type II reactions
A
- Myasthenia gravis
- Rhesus isoimmunisation
- HDN
- Graves
5
Q
What happens in myasthenia gravis?
A
- In healthy individuals, nerve impulses trigger release of Ach from nerve endings, binds to AchR on muscle cells triggering contraction
- In MG, autoantibodies to AchR are produced. These block the AchR at the postsynaptic NMJ, diminishing muscle contraction
- Causes muscle atrophy
6
Q
What happens in Rhesus isoimmunisation?
A
- RhD Ag is carried on RBCs
- If RhD-ve mother has baby with RhD+ve father, mother will become sensitised to RhD and make Abs
- In the second pregnancy, if the foetus is Rh+ve, small amounts of RBCs crossing placenta stimulate memory cells
- This causes production of more anti-RhD Abs, which cross the placenta and cause HDN
7
Q
What happens in Grave’s disease?
A
- Autoantibodies are made that act on TSHR on thyroid
- Causes lots of TH to be made
8
Q
What happens in myasthenia gravis?
A
- In healthy individuals, nerve impulses trigger release of Ach from nerve endings, binds to AchR on muscle cells triggering contraction
- In MG, autoantibodies to AchR are produced. These block the AchR at the postsynaptic NMJ, diminishing muscle contraction
- Causes muscle atrophy
9
Q
What causes a type II reaction?
A
Ag and Ab interaction of IgM
10
Q
What is a type IV reaction?
A
- Delayed hypersensitivity
- T-cell mediated but DCs, macrophages and cytokines contribute to process
- e.g. Mantoux test, Type 1, coeliac, IBD, Crohns, psoriasis
11
Q
What happens in myasthenia gravis?
A
- In healthy individuals, nerve impulses trigger release of Ach from nerve endings, binds to AchR on muscle cells triggering contraction
- In MG, autoantibodies to AchR are produced. These block the AchR at the postsynaptic NMJ, diminishing muscle contraction
- Causes muscle atrophy
12
Q
Define a type III reaction
A
- Type III target is soluble circulating Ag
- Ag can be own tissue or foreign material
- e.g. SLE
13
Q
What happens in SLE?
A
- Aetiology unknown, but familial pattern
- Make autoantibody directed against self molecules including DNA and nuclear ribonucleoproteins
- Forms immune complexes - get trapped in kidney and cause glomerulonephritis
- The Abs can fix complement - tissue injury
- Abnormal activation of B cells - more sensitive to stimulatory cytokines
- Reduced Th1 response
- probs with phagocytes mean that they cant clear immune complexes
14
Q
What is a type IV reaction?
A
- Delayed hypersensitivity
- T-cell mediated but DCs, macrophages and cytokines contribute to process
- e.g. Mantoux test, Type 1, coeliac, IBD, Crohns, psoriasis
15
Q
What is the mantoux test?
A
- TB vaccine test
- Inject pt with extract of mycobacterial Ag in skin
- Macrophages present ag to activate Th cells - release cytokines to activate macrophages, which release cytokines
- Red swelling of skin
16
Q
What components can lead to immundeficiency?
A
- complement - C1q inhibitor deficiency -> hereditary angioedema (continuous complement activation)
- C3 deficiency -> infection
- Phagocytes - Chediak-Higashi (failure of phagolysosome formation and lysosome degranulation)
- B cell deficiencies - SCID (lack of development of stem cells into B or T cells)
- Hyper IgM (increased IgM but little or no IgG)
- Common variable immunodeficiency (IgG/A deficiency - B cells unable to mature into plasma cells)
- T cell deficiencies
- Lack of thymus -> DiGeorge
17
Q
What happens in coeliac?
A
- Small intestine disease
- HLA type imortant
- Patients have IgA anti-gliadin, antiendomysium and antireticulin Abs
- T cells present in intestine
- Causes villous atrophy
- Leads to malbsorption
18
Q
What causes psoriasis?
A
- Chronic skin disease - red plaque with silvery scales
- Genetic and environmental factors
- lots of CD4+ cells in skin
- Immunosuppressive treatment is effective
19
Q
What factors contribute to development of autoimmune disease?
A
- Age and gender (autoantibodies more common in elderly, SLE and Grave more common in women)
- Drugs
- Immunodeficiency
20
Q
What components can lead to immundeficiency?
A
- complement - C1q inhibitor deficiency -> hereditary angioedema (continuous complement activation)
- C3 deficiency -> infection
- Phagocytes - Chediak-Higashi (failure of phagolysosome formation and lysosome degranulation)
- B cell deficiencies - SCID (lack of developmnt of stem cells into B or T cells)
21
Q
What can cause secondary immunodeficiency?
A
- HIV infection - AIDS
- Malnutrition
- Tumours - cancerous cells can release immunosuppressive factors
- Cytotoxic drugs/ radiation
