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The potential physiological mechanisms explaining an influence of psychosocial stress on autoimmune diseases remain undetermined. Exposure of chronic social isolation stress to MRL/lpr mice significantly enhanced the degree of proteinuria after 20 weeks of age and reduced the survival rate. The serum anti-dsDNA IgG2a levels were increased significantly by stress at 19 weeks of age, which was simultaneously accompanied by inhibition of the serum corticosterone elevation. Furthermore, stress caused increased IFN-gamma production from anti-CD3-stimulated splenic mononuclear cells, whereas IL-4 and IL-10 production decreased. These results indicated that isolation stress exacerbated autoimmune disease in MRL/lpr mice, the possible mechanism for which might be related to stress-induced dysregulation of Th1/Th2 balance and inhibition of the blood corticosterone response to inflammatory stimuli.

The skin response to myelin basic protein (MBP) was studied in chronic relapsing experimental allergic encephalomyelitis (EAE) using strain 13 guinea pigs. The delayed type skin response showed a monophasic curve; it gradually increased after immunization, reached maximum levels around 80 days post-immunization, and decreased thereafter. Relapses were more frequent while it was at high levels although it did not correlate directly in individuals with the clinical stage. The skin response was also high in MBP-immunized animals which had recovered from acute EAE. Our results suggest that delayed type hypersensitivity to MBP is involved but is not sufficient by itself to cause relapsing EAE.