Hypersensitivity and Autoimmunity Flashcards
Type 1 hypersensitivity
Body recognises an environmental antigen as a pathogen
Releases IgE and triggers mast cell responses
Allergen shown to T helper cell during sensitisation – causes B cells to differentiate and produce IgE against the antigen
Results in allergic reaction every time there is exposure to the antigen due to release of antigens from mast cells
Type 2 hypersensitivity
Antibodies bind to own antigens
IgG and IgM trigger the complement system causing cell lysis
Type 3 hypersensitivity
Low concentration of antibody coupled with large concentration of antigen causes small immune complexes to form
Type 4 hypersensitivity
CD4 helper T cells recognise the foreign antigen, and start to produce cytokines which leads to an inflammatory response
Atopy
A state of sub-clinical immune sensitisation (the presence of IgE with no related symptoms)
Early phase allergic reactions
Occurs within minutes, performed by mast cell mediators (histamine, heparin, chemotactic factors)
Late phase allergic reactions
Newly synthesised mediators (Prostaglandins, leukotrienes)
Th2 cytokines
Eosinophil mediators
Localised type 3 hypersensitivity
Causes localised inflammation and can be cleared away by macrophages
Systemic type 3 hypersensitivity
Complexes are deposited in tissues and organs such as the skin, joints, kidneys and blood vessels
Immunological tolerance
Through deletion of autoreactive T and B cellsduring maturation or by inhibiting the activity of the autoreactive cells which escape the central tolerance process
Pathogenic mechanisms in autoimmune disease
Cell-mediated
Antibody-mediated
Immune complex-mediated
Recruitment of innate compounds
Organ specific autoimmune disease
Thyroid
Stomach
Adrenal
Non-organ specific autoimmune disease
Muscles
Skin
Kidneys
Joints
