The a b i l i t y o f androgens t o suppress and estrogens t o accelerate murine lupus o f f e r s an explanation f o r t h e marked female predominance o f systemic lupus erythematosus (SLE). New i n f o r m a t i o n i s presented on t h e possible mechanisms whereby sex s t e r o i d hormones can modulate autoimmune disease. The nonlymphoid elements t h a t help c o n t r o l immune responses, such as thymic e p i t h e l i u m and c e l l s o f t h e r e t i c u l o e n d o t h e l i a l system, may be important t a r g e t s i t e s f o r sex s t e r o i d hormone action.
This i s suggested by t h e presence of sex s t e r o i d hormone receptors on thymic epithelium, and by the a b i l i t y o f sex s t e r o i d hormones t o i n f l u e n c e t h e clearance o f p a r t i c u l a t e immune complexes.
A l l autoimmune susceptible mice have a d e f i c i e n c y o f I n t e r l e u k i n -2 (IL-2), a l s o known as T C e l l Growth Factor.
I n two s t r a i n s (MRL and C57BL6), t h i s IL-2 d e f i c i e n c y i s associated w i t h t h e presence o f the l p r gene which i s responsible f o r autoimmunity and lymphop r o l i f e r a t i o n . Both MRL-lpr and C57BL6-lpr mice have a decreased c a p a c i t y t o produce and respond t o IL-2. The a b i l i t y o f androgen t o ameliorate autoimmune disease i n NZB/NZW F (B/W) mice i s associated w i t h maintenance o f IL-2 a c t k i t y .
These r e s u l t s suggest t h a t IL-2 i s an important immunoregulatory molecule whose d e f i c i e n c y may l e a d t o disturbances i n immunologic c o n t r o l mechanisms and perhaps t o immunoregulatory diseases such as SLE.