Abstract :
Autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, or scleroderma have been considered to represent disorders associated with reaction of the patientʹs own immune system against self-antigens or body systems. In many such disorders, tissues involved show lesions or morphology indicating destructive inflammatory or reactive features clearly produced by or associated with cell-mediated or antibody-driven reactions of the patient against his own tissues. After an exhaustive search which has stretched back in time for at least the last five decades, we seem to understand how the immune system works better than previously. However, despite the fact that we now understand molecular mechanisms of antibody selection and structure, how the cell-mediated and humoral antibody system is activated in terms of signal peptides and in the context of HLA molecules, we have not yet exactly identified inciting antigens which clearly cause these diseases.
The focus recently has shifted towards being able to down-modulate potentially harmful parts of a self-directed inflammatory process by abrogating harmful messenger molecules participating in tissue injury. Following such a path, we may actually alleviate or cure these diseases before eventually identifying their original cause.
