DIETARY VITAMIN-A-DEFICIENCY AND THE IMMUNE-SYSTEM IN A MURINE MODEL OF SYSTEMIC LUPUS-ERYTHEMATOSUS

The purpose of this study was to investigate the effects of dietary vi tamin A deficiency on the onset and progression of systemic lupus eryt hematosus (SLE), a severe autoimmune disorder, using the murine SLE mo del, MRL/MPJ-lpr/lpr (MRL/l) mice. Sixty weanling female 4-week old MR L/lpr mice were randomly assigned to either the vitamin A-deficient (A (-)), A-sufficient (A(+)), and A-sufficient diet/feed restricted (DR) groups. The weight losses due to the onset of SLE for both the A+ and the DR groups were greater than that for the A- group (P<0.01 at 16 we eks of treatment or 24 weeks of age). Both thymus and spleen weights a s the percentage of body weights for the A- group were lower than thos e for the A(+) and the DR groups within 12 weeks of diet treatment (or 20 weeks of age). The degree of the abnormality in splenocyte composi tion, viz. an increased ratio of Thy 1.2 (total T cells) and a relativ ely decreased ratio of SmIg positive splenocytes (total B cells), was more severe in both the A(+) and the DR groups than in the A(-) group. This change suggests that vitamin A deficiency may suppress the proli feration of abnormal T splenocytes in MRL/l mice. The results of T and B splenocyte proliferation stimulated by mitogens, either concanavali n A (Con A) or lipopolysaccharide (LPS) in vitro, indicated that vitam in A deficiency exerted a suppressive effect on the activities of abno rmal T and B splenocytes of MRL/l mice. The deficiency of vitamin A in the diet also suppressed serum anti-DNA autoantibody production in MR L/l mice. In summary, it caused a suppression in autoimmunity as expre ssed by a decreased hyperactivity in both cellular and humoral immune functions in MRT/l mice. The overall res;lts suggest that dietary vita min A deficiency retarded the progression of SLE and resulted in a bet ter survival of MRL/l mice.