Direct effect of interleukin 2 on the differentiation of human B cells which have not been preactivated in vitro.

Direct effect of interleukin 2 on the differentiation of human B cells which have not been preactivated in vitro.
复制标题

白细胞介素2对体外未预激活的人B细胞的分化有直接影响。

DOI:
10.1002/eji.1830151102
复制
发表时间:
1985
影响因子:
5.4
通讯作者:
Fauci,AS
Fauci,AS
中科院分区:
医学3区
文献类型:
--
作者:
LethiBich-Thuy;Fauci,AS

文献摘要

相似文献

重组白细胞介素2(IL 2)可诱导人扁桃体B细胞分化,而不需要体外预激活信号。这些细胞悬液在培养开始和终止时均不含可检测的T细胞、单核细胞或自然杀伤细胞,并且对T细胞依赖性多克隆B细胞活化剂美洲商陆有丝分裂原无应答。在不存在IL 2的情况下,在培养开始和结束时,它们含有非常少的Tac抗原携带细胞(小于2.5%)。在存在IL 2的情况下,仅观察到Tac抗原携带细胞数量的极轻微增加。观察到的分化并不是由于污染T细胞的影响,因为故意污染高达5% T细胞的培养物并不比不添加T细胞的培养物含有更多的IgM、IgG或伊加。此外,当T细胞以IT细胞/9个B细胞的比例存在时,IgM的产生减少。综上所述,这些数据支持以下假设:(a)B细胞对IL 2的反应性分化可能在没有体外预活化的情况下发生,在这种情况下,与B细胞表面Tac抗原的表达无关;(B)它不是由于极少量的T细胞的辅助效应可能污染B细胞悬浮液;和(c)它很可能是由IL 2对B细胞本身的直接作用引起的。这些数据还指出,在IL 2存在的情况下,T细胞可能对IL 2诱导的B细胞分化产生抑制作用,而不是提供辅助信号。
Unfractionated as well as small and large human tonsillar B cells were found to differentiate in the presence of recombinant interleukin 2 (IL 2) without requiring anin vitropreactivation signal. These cell suspensions did not contain detectable T cells, monocytes or natural killer cells both at the initiation and the termination of cultures, and did not respond to the T cell‐dependent polyclonal B cell activator pokeweed mitogen. They contained very few Tac antigen‐bearing cells (less than 2.5%) at the beginning and at the termination of the cultures in the absence of IL 2. In the presence of IL 2, only a minimal increase in the number of Tac antigen‐bearing cells was noted. The observed differentiation was not due to the effects of contaminating T cells, since cultures purposely contaminated with up to 5% of T cells did not contain greater amounts of IgM, IgG or IgA than cultures without T cells added back. Furthermore, when T cells were present at a ratio of IT cell per 9 B cells, the production of IgM was decreased. Taken together, these data support the hypothesis that (a) B cell differentiation in response to IL 2 may occur in the absence ofin vitropreactivation, and in this case cannot be related to the expression of Tac antigen on the B cell surface; (b) it is not due to helper effects of very low numbers of T cells which might contaminate the B cell suspensions; and (c) it most likely results from a direct effect of IL 2 on B cells themselves. The data also point out the fact that, in the presence of IL 2, T cells may trigger inhibitory effects on IL2‐induced B cell differentiation rather than provide helper signals.