Immunology in pathology (immunopathology) Patology. immunology in pathology. immunologic response. lecture 3

Transcription

1 Patology Immunology in pathology (immunopathology) lecture 3 prof. dr hab. n. med. Andrzej Marszałek immunology in pathology Diseases with immunologic mechanism of tissue injury. Hypersensitivity reactions: Type I Type II Type III Type IV Amyloidosis immunologic response

2 - surface barriers - phagocytosis: - neutrophils - macrophages - NK cells - serum proteins - eg. complement elements - lectins binding mannose - C-reactive protein - TLR receptors phagocytosis lymphocytes/ NK cells antibodies

3 disorders of the immune system hypersensitivity reactions autoimmune disease immunologic deficiency syndromes amyloidosis hypersensitivity reactions type I hypersensitivity type I hypersensitivity develops rapidly after the combination of an antigen with antibody (IgE) bound to mast cells or bazophils. when IgE bounds to alergen it leads to: realese of vasoactive amins and mediators which have influence on vascular permeability, constriction of smooth muscle cells in many organs, realese of cytokines, which provoke inflow of inflammatory cells - anaphylaxis - allergies - bronchial asthma (atopic forms) production of IgE - vascular dilatation immediate release of - edema vasoactive amines - smooth muscle and other mediators contraction from mast cells; recruitment of - mucus production inflammatory cells - inflammation (late-phase reaction)

4 type II hypersensitivity type II hypersensitivity Diseases mediated by antibodies Pathologic changes are caused by humoral antibodies, which bind to antigens on the tissue surface or cell surface leading to processes which increase susceptibility of cell to phagocytosis or lysis caused by complement system. -Autoimmune hemolytic anemia -Goodpasture syndrome Production of IgG, IgM binds Ag on target cells/tissues phagocytosis or lysis of target cells by activated complement or Fc rec.; recruitment of leukocytes - cell lysis -inflammation type III hypersensitivity type III hypersensitivity immune complex disease ; antibodies binds to antigens forming complexes, which deposits in vascular wall and activate complement system. immune complexes and fragments of activated complement attract neutrophils and monocytes. Finally in immune complexes diseases activated complement and enzymes and other toxic molecules (e.g.. oxygen metabolites) released from neutrophils cause tissue damage. -SLE -Arthusa reaction -some GN -serum sickness Deposition of Ag-Ab complexes complement activation recruitment of leukocytes complement products or Fc. rec. release of enzymes or other toxic molecules -necrotizing vasculitis (fibrinoid necrosis) -inflammation

5 type IV hypersensitivity type IV hypersensitivity delayed type hypersensitivity cell mediated hypersensitivity diseases caused by cell mediated response in which tissue and cell injury is initiated by antigen-sensitized T lymphocytes -tuberculosis -transplant rejection -DM type I -multiple sclerosis -Contact dermatitis Activated T lymphocytes i) release of cytokines and macrophage activation -perivascular cellular infiltrates -edema -cell destruction -granulomas ii) T cell-mediated cytotoxicity autoimmune diseases rare (about 5%), with exception RA autoimmunologic thyroiditis activation of T and B lymphocytes without infection slight autoreactivity is physiologic

6 scleroderma) generalized abnormality in Fas protein or its receptor demyelinization syndromes after Campylobacter jejuni infection autoreactive lymphocytes B producing autoantibodies against ganglioside Guillain-Barré syndrome over activation of T lymphocytes by jejunal flora inflammatory bowel disease (IBD) transplant rejection amyloidosis

7 amyloidosis group of desesaes tissue deposits of insoluble β-plited protein deposits deposits reveal yellow-green birefringence in polarizing microscope