[Animal models in lupus]

The study of spontaneous animal models of the lupoid disease has permitted a better understanding of the intermediary mechanisms which lead to the production of auto-anti-polymorphonuclear antibodies, and of glomerulo-nephritis by means of immune complexes. In comparison with a primitive thymic deficiency which causes a disorder in immunity regulation, under the control of activating and suppressing T lymphocytes, these models have demonstrated the probable role of intrinsic hyper-activity of the B lymphocytes. The association of these two disturbances seems necessary for the development of the disease in NZB and F1 New Zealand mice (NZB X NZW); nonetheless, the studies of other murine models (notably MRL/1 pr and B X SB mice) reveal a great diversity in lymphocytic disturbances, capable of leading to the production of auto-antibodies. These models allow genetic control of lupoid disease to be undertaken. Finally, canine lupus and Aleutian mink disease underline the possible role of a transmittable viral agent.