In humans systemic lupus erythematosus (SLE is an autoimmune disease o
f unknown etiology. According to many studies, the disease depends on
genetic and environmentally acquired factors, and preferentially occur
s in females. The MRL/lpr mouse is a good model of human SLE since mos
t of the pathologic expressions associated with the human disease (e.g
. skin lesions, lymphadenopathy, arthritis, nephritis, multiple autoan
tibodies etc.) also occur in the mouse. MRL/lpr mice were orally suppl
emented 5 times/week with 0.4 mg vitamin E/day and compared with mice
on a commercial or a vitamin E-deficient diet. The results were: the m
ean survival time was extended; the massive spleen and lymph node enla
rgements were reduced; mitogenic responses of T and B cells stimulated
with concanavalin A or lipopolysaccharide were enhanced; the abnormal
differentiation patterns of thymic and splenic subpopulations were ch
anged; the oxidative burst of splenic macrophages was increased; titer
s of anti-double stranded DNA antibodies, concentrations of serum amyl
oid protein (SAP, an acute phase protein), and proteinuria were reduce
d. Vitamin E administration produced a definite amelioration, but not
an absolute cure of the chronic SLE-like disease. The results indicate
that vitamin E beneficially influences the development of the SLE-lik
e disease in MRL/lpr mice, which suggests a possible measure to reduce
human SLE and probably various other autoimmune diseases in humans.