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Human B cell growth factors overcome T cell-mediated inhibition of specific antibody production: a possible mechanism for the exacerbation of autoimmune disease.

机译:人类B细胞生长因子克服了T细胞介导的特异性抗体产生的抑制作用:一种可能加剧自身免疫性疾病的机制。

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摘要

Under normal circumstances, antigen-dependent antibody production in man requires autologous T cells, B cells and macrophages. If allogeneic T cells are substituted, then antibodies are not synthesized, due to the development of inhibitory interactions. Addition of B cell growth and differentiation factors changes this pattern of response, and allows antibodies to be produced even when allogeneic T cells are the source of help. There is evidence that such B cell growth factors are released during most normal immune responses: we suggest that their ability to allow B cells to escape from inhibitory interactions and secrete antibodies, may underlie the observed exacerbation of certain autoimmune diseases by intercurrent infection.
机译:在正常情况下,人体内抗原依赖性抗体的产生需要自体T细胞,B细胞和巨噬细胞。如果同种异体T细胞被取代,则由于抑制性相互作用的发展,抗体将无法合成。 B细胞生长和分化因子的添加改变了这种应答方式,即使异体T细胞是帮助的来源,也可以产生抗体。有证据表明,这种B细胞生长因子在大多数正常的免疫应答过程中被释放:我们建议它们允许B细胞逃脱抑制性相互作用并分泌抗体的能力,可能是由于并发感染导致某些自身免疫性疾病加剧的基础。

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