Evidence from a variety of sources supports the notion that stress and emotional distress may relate to dysfunction and hypofunction of the immunologic system. We have experimental evidence that some forms of stress reduce primary and secondary antibody response to low dose antigen stimulation in rats and that adult immunologic responsivity may be altered by early infantile experience. Mixed-sex group housing at high male-female ratios increases severity of adjuvant-induced arthritis in the male rat. Graft-versus-host reactions are diminished by food-limitation stress to recipient animals. Sex segregated group-housed mice show larger murine virus-induced sarcomas when inoculated at 6 and 9 months of age than males housed individually with two or more females. Electric shock stress for 3 days prior to inoculation with virus reduces incidence and size of MSV tumors, while shock administered 3 days following inoculation increases tumor size. Female mice that develop spontaneous fighting behavior show significantly greater resistance to MSV tumors. Acutely ill schizophrenic patients with relatively high levels of IgA and IgG have a poorer short-term prognosis. Electrolytic lesions of the ventromedial and posterior nuclei of the hypothalamus of recipient and possibly also of donor animals impair the GVH reaction. Our experimental findings suggest that stress and central nervous system lesions affect thymus-derived lymphocytes (T-cells) and play a role in cell-cell interaction or the release of mediators from reacting lymphocytes. Ultimately, we may find that stress affects the macrophage, a hormone-sensitive cell that plays a role in afferent, central and efferent limbs of the immune system.

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