Autoimmunity mechanisms underlying

The typical pancreatic lesion of type 1 diabetes is the selective loss of almost all 3-cells, whereas other islet cell types (a, 8, and pancreatic polypeptide cells) remain intact. The most common mechanism for 3-cell destruction is thought to be autoimmune-mediated inflammatory damage. Prospective family studies strongly support a genetic basis for susceptibility to this autoimmune process and suggest that the underlying immune abnormalities precede clinical insulin deficiency by many years. However, not all spontaneous type 1 diabetes is the result of autoimmune mechanisms. 

The complex mechanisms underlying inflammation control and its implication in various pathologies have been delineated in this overview. The full comprehension of these mechanisms is necessary to indicate a path for experimenting new treatments for the control of inflammation. The challenge being that of controlling chronic inflammatory processes, at the basis of diseases such as atherosclerosis, neurodegenerative and autoimmune diseases. 

Immunotoxicity deals with immune dysfunction resulting from exposing an organism to a xenobiotic and explores the mechanisms underlying these effects in a biological system. The immune dysfunction may take the form of immunosuppression or, alternatively, exaggerated immune reaction such as allergy, autoimmunity, or... 

Pathophysiologically, there is little difficulty in recognizing disseminated intravascular coagulation and then treating this on merit. Much more frequent are immunologically mediated mechanisms that may be secondary to underlying collagen-vascular diseases such as systemic lupus erythematosus or where the defect exists in isolation and the process is defined as primary, idiopathic or autoimmune. 

---