10. immunological diseases Flashcards
immunological diseases
immune system may fail to control infection
immune system may cause disease directly
gell and coombes classification
refers to mechanisms of disease where immune system is inappropriately activated
gell and coombes types
type I - IgE antibody, allergy
type II - pathogenic antibody
type III - antibody-antigen complex
type IV - t cell mediated
type I hypersensitivity
IgE mediated allergy
B cells class switch to IgE antibody - picked up by tissue mast cells and circulating basophils
cross linking of allergen specific IgE antibodies by allergen activates the cell
mast cell rapidly degranulates - releases histamine, tryptase etc
type II hypersensitivity
pathology directly mediated by antibodies
eg mismatch blood transfusion reactions
IgM antibodies against AB antigens develop during first year of life
antibodies = isoantibodies (detect similar antigens on surface of gut bacteria and cross-react with red cell antigens)
haemolytic disease of the newborn
type II hypersensitivity
majority of population is D+ (rhesus)
mother may be exposed to other, and make antibodies for rhesus group
antibodies may cause disease in subsequent pregnancies
what can autoimmune haemolysis do to a foetus?
growth retardation
cardiovascular
‘hydros fettles’
neurotoxicity form high bilirubin levels
type III hypersensitivity
disease caused by complexes of antibody-antigen complex
usually soluble, removed in spleen
can become insoluble in some situations and cause disease
eg large quantity of antigen or antibody, strong interaction, complexes large
local immune complex disease
type III hypersensitivity
painful lesions in fingertip pulp - deposition of circulating immune complexes
maybe seen in infective endocarditis (Osler’s nodes)
may be seen in other diseases with immune complex deposition, eg SLE
serum sickness
type III hypersensitivity
generalised, transient immune complex-mediated syndrome
mainly results from injection of certain immunogenic drugs /anti sera produced in animals
rash, fever, arthritis, glomerulonephritis
hypersensitivity pneumonitis
type III hypersensitivity
also known as extrinsic allergic alveoli’s (EAA)
patient becomes sensitised to environmental antigen by repeated exposure, producing large quantities of IgG
immune complexes form int he lung upon re-exposure - shortness of breath and cough
initially transient, lung scarring with repeated exposure
type IV hypersensitivity
reactions mediated by antigen-specific effector T cells
takes time to process and present antigen: reactions develop >24 hours after exposure
known as contact dermatitis in skin
contact dermatitis sensitisation
sensitising agents are typically highly reactive small molecules which penetrate skin
react with self protein-hapten complexes - picked up by Langerhans cells which migrate to lymph nodes langerhans cells process and present antigen together with MHC iI
activated T cells migrate to dermis
tuberculin skin test (TST)
type IV hypersensitivity
used to determine previous TB exposure
tuberculin injected intradermally ]local inflammatory response evolves over 24-72 hours if previously exposed
mediated by Th1 cells
mechanism of TST
antigen is injected into subcutaneous tissue
processed by local antigen presenting cell s
th1 effector cell recognises antigen
releases cytokines, act on vascular epithelium
recruitment of phagocytes and plasma to site
visible lesion
