TYPE 3 (IMMUNE COMPLEX MEDIATED)HYPERSENSITIVITY-Pathogenesis-Causes-Effects-Diseases
Ag = Antigen
Ab= Antibody
Ag-Ab complexes formation is a normal phenomenon in most of the situations but they do not deposit normally. It is the size of the complexes or the functional or structural abnormality of the mononuclear phagocytic cells which render the Ag-Ab complexes to be deposited in various locations. Charge and three-dimensional structure of the immune complexes, the valency of the Ag, the affinity of the Ag to various tissue components and hemodynamic factors also play roles in the deposition of the complexes.
PATHOGENESIS (Mechanism) OF TYPE III (IMMUNE COMPLEX MEDIATED)HYPERSENSITIVITY
Type III hypersensitivity diseases may be systemic or local. In both of them the pathogenesis is divided into three phases:•The first phase (formation of Ag-Ab complexes): In this Ag enters the body interacts with the immunocompetent cell which produces Abs against that Ag. This process takes about one week. The Abs react with the Ag in circulation and form Ag-Ab complexes.
•The second phase (Deposition of circulating complexes): In this phase the circulating complexes deposit in various tissues.
•The third phase (acute inflammatory reaction): in this phase acute inflammatory reaction is initiated by activation of the complement cascade which in response activate neutrophils and monocytes
through their Fc receptors. This phase is represented by fever, urticaria, arthralgias, lymph nodes enlargement and proteinuria.
•Antigen/Antibody “Complexes” mainly deposit in the:
–Kidney (Glomerular Basement Membrane)–Blood Vessels, Skin and Joints
Common Type III Diseases:-
Systemic Diseases:
SLE, Polyarteritis nodosa, Post-streptococcal glomerulonephritis, Serum sickness (days).Local diseases:
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