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Abstract-We investigated the correlation between restraint stress-induced alter ation of antibody responses and adrenal hormones. Adrenalectomy (Adx) blocked both the suppression of antibody response against T cell-dependent (TD) antigen and the enhancement of that against T cell-independent (TI) antigen in stressed mice. Adx also inhibited the atrophy of both thymus and spleen caused by restraint. Pre-treatment of metyrapone, an inhibitor of adrenocortical steroid biosynthesis, had an effect that was similar to, but far weaker than that of Adx on stressed mice. The pre-administration of phenoxybenzamine, an a-adrenergic blocking agent, to mice prevented both the inhibition of antibody response to TD antigen and the decrease in spleen cell number of restrained mice. A similar effect was observed in mice pre-treated with 6-hydroxydopamine, an adrenergic neuron degenerating agent.However, no effects of these two agents were observed on the enhancement of antibody response to TI antigen. The suppressive effect of the antibody response to TD antigen was augmented by the pre-administration of propranolol, a e3-adrenergic blocking agent. These results suggest that the suppression of the function of T cells in restrained mice are attributed to the released adrenocortical and adrenal medullary hormones and activated sympathetic nervous system and that the enhance ment of B cell function is due to the adrenocortical hormones.

Abstract-Effectsof restraint stress on humoral immune responses were investi gated in mice. Mice were restrained for 12 hours per day at nighttime and released at daytime for 2 consecutive days, either before or after sheep red blood cell (SRBC) immunization.The antibody response to SRBC was markedly suppressed in mice that were restrained before antigen injection.In contrast, the response was not significantly affected when the stress was loaded after immunization.Oral admin istration of 10 mg/kg diazepam prevented the stress-induced suppression of anti SRBC antibody response.On the other hand, antibody responses to T cell independent antigens such as trinitrophenylated (TNP)-Ficoll and TNP-lipopolysac charide were not suppressed.These results suggest that the restraint stress causes dysfunction of T cell populations in mice.

Abstract-The influences of restraint stress on the functions of T cells, B cells and adherent cells in antibody responses were investigated. Antibody response against sheep red blood cells (SRBC), a T cell-dependent antigen, in cultured splenocytes from restrained mice was reduced to about 40-50% of that from the control mice. Addition of normal T cells to these cultures, however, restored the suppressed response.Moreover, helper T cell activities were lowered in restrained mice. On the other hand, suppressor T cell activities induced by both concanavalin A (Con A) and SRBC were significantly decreased in restrained mice. However, the antibody responses to T cell-independent antigens in stressed mice were approximately 40% higher than the control response. These enhancemant were also observed in T cell-depleted splenocytes. Polyclonal antibody response induced by lipopolysaccharide (LPS) was increased in stressed mice. Antigen presenting cell activities were little influenced by restraint stress. Proliferative response to Con A, but not that to LPS, was suppressed in splenocytes from restrained mice. These results suggest that both helper and suppressor activities of T cells are suppressed, but B cell activity is rather enhanced in splenocytes from restrained mice.

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TEI-3096 [6-p-chlorobenzyl-5H-2,3,6,7-terahydro-5,7-dioxothiazolo (3,2-a) pyrimidine], a novel thiazolopyrimidine compound has been shown to suppress adjuvant arthritis in rats without any effect on conventional inflammation. We examined the immuno-pharmacological profile of TEI-3096 in murine lymphocytes. The blastformation induced by Con A or LPS was inhibited by addition of 50-500 microM concentrations of TEI-3096. This compound suppressed elevated plaque-forming cell (PFC) response against T cell-dependent antigen. However, TEI-3096 had no effect either on normal PFC response or on antibody formation against T cell independent antigen. Although orally administered TEI-3096 had no obvious effect on anti-SRBC PFC response in normal mice, it normalized the colchicine-induced enhancement of antibody formation against TNP-HGG. TEI-3096 also enhanced the delayed type hypersensitivity in mice and rats. These results suggests that TEI-3096 restores the abnormal immune response. Therefore, it may be useful for the treatment of auto-immune disease such as rheumatoid arthritis.