Immunological disease classifications Flashcards
Gell and Coombes hypersensitivity reactions
Classification of immunologically-mediated diseases.
- Where the immune system is inappropriately activated.
Type 1 hypersensitivity reaction
- Mechanism
- Examples
IgE antibody is directed against allergens
- mast cell degranulation
Examples
- Seasonal arthritis
- Cat allergies
Ig-E mediated allergy
Believed to assist parasite immunity.
Secreted IgE from B cells binds to mast cells/ basophils.
Allergen specific to IgE on mast cell binds and causes cross linking of the receptors.
Mast cell degranulates- releases histamine, tryptase and other mediators
- Leads to symptoms of the affected organ
Type 2 hypersensitivity reaction
- Mechanism
- Examples
Pathology directly caused by antibodies.
Examples
- Autoimmune haemolysis
- Haemolytic disease of the newborn
- Mismatch blood transfusion
Type 2 hypersensitivity reaction: Mismatch blood transfusion
Isoantibodies (IgM) developed against surface antigens of gut bacteria are produced against AB antigens of red blood cells.
Hence why: - Rbc A antigen--> B ab - Rbc B antigen--> A ab - Rbc AB antigen--> No ab Universal recipient
- Rbc no antigen–> AB antibody
Universal donor
Mismatch of blood= Type 2 hypersensitivity
Haemolytic disease of the newborn
T2 reaction.
Mother Rh-, father Rh+ (can have Rh+ baby)
Mother can be exposed to D antigens during trauma/ parturition, if baby is D+.
- Causes mother to produce Ab against D antigens which can cross placenta in later pregnancies.
Ab binds to fetal red cells=haemolysis
- Growth retardation
- CVS failure
- High bilirubin neurotoxicity
Haemolytic disease of the newborn management
If mother is Rh- and partner is Rh+, anti-D IgG is given at 28 weeks routinely.
- IgG blocks fetal rbcs, prevents sensitisation
Reduces risk from 16% to 0.1%
Autoimmune haemolysis
T2 reaction
Autoantibodies develop against rbcs
- auto-Ab-RBC complex is either destroyed via phagocytosis (intersitium) or complement activation (intravascular haemolysis)
Type 3 reactions
Caused by Ab-Ag complexes that become insoluble and cause disease
Due to:
- Large amounts of Ab or Ag
- Very strong affinity between Ab and Ag
- Larger complexes
Examples
- Local immune complex disease
- Serum sickness
- Hypersensitivity pneumonitis
Local immune complex disease
T3 reaction
Deposits of circulating immune complexes in the fingertip pulp
Seen in infective endocarditis (Olser’s nodes), SLE
Serum sickness
T3 reaction
Injection from certain immunogenic drug/ anti-sera from animals causes a transient immune complex disease.
Signs
- Rash
- fever
- Arthritis
- Glomerulonephritis
Hypersensitivity pneumonitis
T3 reaction
Repeated exposure to environmental antigen leads to a large production of IgG ab.
- Mould spores in hay
- Pigeon feathers and still.
IgG forms complexes in the lung
Presentation
- Shortness of breath
- Cough
- Initially transient then scarring when repeated.
Type IV hypersensitivity
Caused by antigen-specific T effector Cells.
Tend to present at least 24 hrs after exposure to antigen
- Takes time to process and present antigen
Example
- Contact dermatitis
Contact dermatitis
- Mechanism of sensitisation
- Examples
T4 reaction
In the skin:
- Highly reactive, small molecule breaks the skin and forms protein-happen 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
Tuberculin skin test
Type 4 hypersensitivity reaction
- Determines previous exposure to TB
Tuberculin injected intradermally
- Causes local inflammation if previously exposed
