ROLE OF ATG POLYCLONAL ANTIBODIES(3)

ANTIBODIES(3)

Burnet has postulated that autoimmunity arises from emergence of “forbidden clones” which make auto-antibody. Our postulate, in contradistinction, is that auto-antibody-producing cells are always present; producing enough autoantibody to remove damaged or aged tissues. In normal’s, the number of such cells is kept in check by normal T-cells. When T-cell function is defective, the “governing system” controlling auto-antibody producing clones fails, and autoimmune disease, mediated in most diseases by cellular immunity, emerges. Drug purpura, drug hemolytic anemia, and drug leucopenia are now classic examples of diseases in which sensitization to a foreign antigen causes destruction of the sensitized individual’s possess cells.

The known association of gamma globulins with circulating antibodies and the infiltration of the diseased thyroid gland with plasma cells and lymphoid tissue (which are known to produce antibodies) suggested that the disease process and the postoperative findings might be explained if it were postulated that these patients were immunized against an antigen in the thyroid gland.