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 vitamin A deficiency on the onset and progression of systemic lupus erythematosus (SLE), a severe autoimmune disorder, using the murine SLE model, MRL/MPJ-lpr/lpr (MRL/1) mice. Sixty weanling female 4-week old MRL/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 weeks of treatment or 24 weeks of age). Both thymus and spleen weights as the percentage of body weights for the A- group were lower than those 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 composition, viz. an increased ratio of Thy 1.2 (total T cells) and a relatively 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 proliferation of abnormal T splenocytes in MRL/l mice. The results of T and B splenocyte proliferation stimulated by mitogens, either concanavalin A (Con A) or lipopolysaccharide (LPS) in vitro, indicated that vitamin A deficiency exerted a suppressive effect on the activities of abnormal T and B splenocytes of MRL/l mice. The deficiency of vitamin A in the diet also suppressed serum anti-DNA autoantibody production in MRL/l mice. In summary, it caused a suppression in autoimmunity as expressed by a decreased hyperactivity in both cellular and humoral immune functions in MRL/l mice. The overall results suggest that dietary vitamin A deficiency retarded the progression of SLE and resulted in a better survival of MRL/l mice.