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睾酮抑制人外周血单个核细胞产生免疫球蛋白。

Testosterone inhibits immunoglobulin production by human peripheral blood mononuclear cells.

作者信息

Kanda N, Tsuchida T, Tamaki K

机构信息

Department of Dermatology, Faculty of Medicine, University of Tokyo, Japan.

出版信息

Clin Exp Immunol. 1996 Nov;106(2):410-5. doi: 10.1046/j.1365-2249.1996.d01-842.x.

DOI:10.1046/j.1365-2249.1996.d01-842.x
PMID:8918592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2200579/
Abstract

We studied the in vitro effect of testosterone on spontaneous immunoglobulin production by human peripheral blood mononuclear cells (PBMC). Testosterone inhibited IgG and IgM production by PBMC both from males and females. The inhibitory effect of testosterone was revealed at doses more than 1 nM, increased dose-dependently, and reached a plateau at 100 nM. At doses < 1000 nM, testosterone did not reduce cell viability. Testosterone treatment reduced IgG production by 59.0% and that of IgM by 61.3% compared with control. Immunoglobulin production by B cells was also suppressed by testosterone, though the magnitude of the suppressive effect on B cells was lower than that on whole PBMC; testosterone-induced decrease of IgG production compared with control was 26.9% and that of IgM was 24.9%. Exogenous IL-6 partially restored the impaired immunoglobulin production of testosterone-treated PBMC; IgG production in testosterone culture was increased by IL-6 from 35.6% to 66.5% of control and that of IgM was also increased from 38.9% to 71.2%, respectively. Testosterone treatment reduced IL-6 production of monocytes by 78.4% compared with control, but neither affected that of T cells or B cells. These results suggest that testosterone may suppress immunoglobulin production of human PBMC directly by inhibiting B cell activity and indirectly by reducing IL-6 production of monocytes. It is thus indicated that this hormone may have protective and therapeutic effects on human autoimmune diseases.

摘要

我们研究了睾酮对人外周血单个核细胞(PBMC)自发产生免疫球蛋白的体外作用。睾酮抑制了男性和女性PBMC产生IgG和IgM。睾酮的抑制作用在剂量超过1 nM时显现,呈剂量依赖性增加,并在100 nM时达到平台期。在剂量<1000 nM时,睾酮不会降低细胞活力。与对照组相比,睾酮处理使IgG产生减少了59.0%,IgM产生减少了61.3%。睾酮也抑制了B细胞产生免疫球蛋白,尽管对B细胞的抑制作用程度低于对整个PBMC的抑制作用;与对照组相比,睾酮诱导的IgG产生减少为26.9%,IgM为24.9%。外源性IL-6部分恢复了睾酮处理的PBMC受损的免疫球蛋白产生;在睾酮培养物中,IL-6使IgG产生从对照组的35.6%增加到66.5%,IgM产生也分别从38.9%增加到71.2%。与对照组相比,睾酮处理使单核细胞的IL-6产生减少了78.4%,但对T细胞或B细胞的IL-6产生均无影响。这些结果表明,睾酮可能通过抑制B细胞活性直接抑制人PBMC产生免疫球蛋白,并通过减少单核细胞的IL-6产生间接发挥作用。因此表明,这种激素可能对人类自身免疫性疾病具有保护和治疗作用。