[New studies on the pathogenesis of lupus erythematosus].

The pathogenesis of the lupus erythematosus results from co-operation of three principles: (1) genetical disposition, (2) increased reactivity of the immune system, (3) different exogenic influences. The genetical disposition is confirmed by family investigations, metabolic disorders and immune anomalies as well as by parallels to animal models. The reaction manner of the immune system is genetically determined. Exogenic factors influence the immune system (behaviour) either as starter or by modifying the genetical material. The most striking humoral immune phenomenon is an immense number of (auto-)antibodies. Investigations of xeroderma pigmentosum as well as with DNA of different antigenity have shown that an increase of the antigenicity is unlikely for this phenomenon. In the serum of patients there were established and partially characterized factors (mitogens, granulocytic adherence-factor) for increasing the immune reactivity. The increase of such factors may be the sequence of a T-suppressor cell-defect. Like-wise no interdigitating cells in systemic lupus erythematosus have been found, cells which may be responsible for the terminal differentiation of T-lymphocytes. The mode of action of exogenic factors is represented and discussed with the example of the UV provocation.