• 1 January 1982
    • journal article
    • research article
    • Vol. 9  (3) , 353-358
Abstract
The development of multiorgan autoimmune disease is considered in a framework of human lymphocyte ontogeny and immune regulation. A hypothesis is presented that accommodates many typical features of the clinical course and laboratory abnormalities of autoimmune disease by assuming the presence of underlying defects in lymphocyte differentiation. Altered production of and response to poietin-like mediators such as interleukins may be responsible for many of these abnormalities and represent prime candidates for further research into the pathophysiology of autoimmune diseases.