10. Overview of Immunological diseases Flashcards
Type I Hypersensitivity Reaction
-Examples
-IgE antibody directed against allergen triggers mast cell degranulation- release of histamines
E.g. Seasonal rhinitis
Cat allergy
Type II Hypersensitivity Reaction
-Examples
-A pathogenic antibody directly causes diseases
antibody mediated disease
E.g. Autoimmune haemolysis- lyses of red blood cells
Type III Hypersensitivity Reaction
-Examples
Antibody-antigen complex-mediated disease
- enlarged complex that is not removed as they should be
Eg. Serum sickness
Systemic lupus erythematosis
Type IV Hypersensitivity Reaction
-Examples
Inflammation directly mediated by T cells
E.g.
Delayed type hypersensitivity
Contact dermatitis (form of eczema) Tuberculin reaction
-takes time for allergy to appear(hours)
Autoimmune Haemolysis
Type 2 hypersensitivity
Autoantibodies develop against rbcs:
igG anti-red cell response produced de novo
can be destroyed by phagocytes (extracellular hamoysis)
or intravascularly in the spleen
clinical presentation- Anaemia , and jaundice due to release of bilirubin
Hypersensitivity pneumonitis
Type III reaction
clinically presents with pts exposed to airbourne (like hay) antigen then develops sudden breathlessness
- produce IgG antibodies
- eventual lung scarring and fibrosis
Tuberculin skin test (TST)
Type IV hypersensitivity reaction
- Used to determine previous exposure to TB
- Tuberculin injected intradermally
- Local inflammatory response evolves over 24-72 hours if prev exposed
Antigen is injected sc and processed by local APC
- TH1 recognizes antigen and releases cytokines
- Recruitment of phagocytes and plasma to site of antigen -Injection causes visible lesion
Universal recipients belong to which blood group
Group AB
Universal blood donors belong to which blood group
Blood Group O
Haemolytic disease of the newborn
- ‘D’ antigen (Rhesus) is a secondary classification
- Majority of the population are D+
- IgG antibodies produced by the mother move through placenta
Rhesus-negative mothers with rhesus+ partner are given anti-D IgG during pregnancy
Local immune complex disease
Type III reaction
deposition of circulating immune complexes
causing painful lesions
also seen in SLE
Serum sickness
Type III reaction
injection of certain immunogenic drugs or anti-sera produced in animals
Presentation: Rash
Fever
Arthritis
Glomerulonephritis
Contact dermatitis: sensitisation
Type IV reaction
In the skin:
Highly reactive, small molecule breaks the skin and forms protein-hapten complex
-Complex is taken up by Langerhan cells which migrates to lymph nodes
-Antigen is processed and presented via MHC II in Langerhan cells- recognised as foreign by T cells
-T cells migrate to dermis=inflammation (IFN-gamma, cytokines)
Examples
- Nickel
- Perfume/ cosmetic molecules
Interferon gamma release assay (IGRA)
Previous Tb exposure:
Th1 cells recognise antigen. Because this is a secondary immune response, they are ‘primed’ and release cytokines within this short timeframe
No previous Tb exposure:
No primed memory T cells specific for MTB. No interferon gamma produced in such a short timeframe
Gell and Coombes
Pros and Cons
useful framework
- oversimplifies immunology
- not particularly used