Allergy
disease following a response by the immune system to an otherwise innocuous antigen
Hypersensitivities
harmful immune responses that produce tissue damage
type 1 hypersensitivity reaction
immune reactant: IgE
antigen: soluble
Effector mechanism: mast cell activation
example: allergy,asthma
Type II Hypersensitivity
what ca be caused by a penicillin allergy
hemolytic anemia
Type III hypersensitivity
caused usually by IgG but sometimes IgM:
• Formation of antibody-antigen complexes is a normal part of immune response.
• Usually cleared by reticuloendothelial system (RES): macrophages, neutrophils in liver spleen and bone marrow that ingest and degrade immune complexes
• Excess immune complex deposition in tissues leads to pathology
Type III: sites of immune complex deposition: glomeruli
kidney, filtration process makes it very common site in IC deposition, damage driven by complement activation
Type III: sites of immune complex deposition: blood vessel walls
IC accumulate on veins and arteries, causes vasculitis, often seen as skin lesions if close to surface
Type III: sites of immune complex deposition: Synovial membranes:
Rheumatoid arthritis, in which the IgG of the immune complexes can become an antigen itself, and IgM Rheumatoid Factor antibodies develop.
Type III: sites of immune complex deposition: Skin
common site for IC deposition, causes rashes.
Type III: sites of immune complex deposition: systemic sites
in case of Systemic Lupus Erythematosus (SLE) IC deposits in kidney, joints, skin, vasculature, muscle and other organs.
Type IV Hypersensitivity
these are entirely cell mediated, Most Type IV reactions are caused by CD4+ delayed type hypersensitivity (DTH) reactions. ‘Delayed’ refers to reaction occurring 2 to 4 days after antigen exposure
• Macrophages that cause damage are not specific, harm infected and non-infected tissue
DTH reactions
Contact sensitivities of DTH reactions