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多克隆B细胞反应性的T细胞调节。II. 具有X连锁B淋巴细胞缺陷的小鼠T细胞功能缺陷的证据。

T cell regulation of polyclonal B cell responsiveness. II. Evidence for a deficit in T cell function in mice with an X-linked B lymphocyte defect.

作者信息

Goodman M G, Weigle W O

出版信息

J Immunol. 1979 Dec;123(6):2484-7.

PMID:315424
Abstract

In addition to the x-linked B cell maturation deficit previously reported in CBA/N mice, a functional T cell defect has now been observed. T lymphocyte regulation of the polyclonal PFC response was studied within the context of this x-linked immunodeficiency model. The ability of 1) B cells from (CBA X CBA/CaJ)F1, male mice to respond to nonspecific T cell helper signals and 2) T cells from NCF1 male mice to provide such signals was investigated under in vitro conditions by using bacterial lipopolysaccharide (LPS) as the polyclonal activator. B lymphocytes from both male and female NCF1 mice were receptive to T cell help rendered by NCF1 female T cells. Male T cells. however, were unable to augment polyclonal B cell responses of either NCF1 male or female B cells to LPS. Treatment with ATS + C reduced the polyclonal response of female but not male spleen cells to LPS. This deficit could not be overcome by the use of greater numbers of NCF1 male T cells. The observation that this deficiency in T cell regulation is not due to active suppression suggests that the results may be attributable to an intrinsic T cell defect.

摘要

除了先前在CBA/N小鼠中报道的X连锁B细胞成熟缺陷外,现在还观察到功能性T细胞缺陷。在这种X连锁免疫缺陷模型的背景下,研究了T淋巴细胞对多克隆PFC反应的调节作用。在体外条件下,使用细菌脂多糖(LPS)作为多克隆激活剂,研究了1)(CBA×CBA/CaJ)F1雄性小鼠的B细胞对非特异性T细胞辅助信号的反应能力,以及2)NCF1雄性小鼠的T细胞提供此类信号的能力。来自雄性和雌性NCF1小鼠的B淋巴细胞都能接受NCF1雌性T细胞提供的T细胞辅助。然而,雄性T细胞无法增强NCF1雄性或雌性B细胞对LPS的多克隆B细胞反应。用抗胸腺细胞血清+补体(ATS+C)处理可降低雌性而非雄性脾细胞对LPS的多克隆反应。使用更多数量的NCF1雄性T细胞无法克服这种缺陷。T细胞调节缺陷并非由于主动抑制这一观察结果表明,结果可能归因于内在的T细胞缺陷。

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