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原发性同种异体反应性T细胞克隆产生淋巴因子:在七种淋巴因子检测中对233个克隆的协同分析。

The production of lymphokines by primary alloreactive T-cell clones: a co-ordinate analysis of 233 clones in seven lymphokine assays.

作者信息

Sanderson C J, Strath M, Warren D J, O'Garra A, Kirkwood T B

出版信息

Immunology. 1985 Dec;56(4):575-84.

Abstract

A total of 233 primary alloreactive T-cell clones have been tested for the production of interleukin-2 (IL-2), interleukin-3 (IL-3), immune(gamma) interferon (IFN) and granulocyte-macrophage colony-stimulating factor (CSF-2), B-cell growth factor I and II (BCGFI, BCGFII), and eosinophil differentiation factor (EDF). EDF was assayed by means of the eosinophil differentiation assay (EDA). Two principal correlations were observed: IL-3 was shown to be the major lymphokine detected in the bone marrow proliferation assay (BMPA) used to detect CSF-2, and there was a high correlation between the EDA and BCGFII. Subsequent work has suggested that this latter correlation is because a single factor is responsible for both activities. Apart from these two exceptions, and low level correlations probably due to the fact that different assays detect more than one lymphokine, there was no evidence for co-ordinate expression of lymphokines. There was a large variation in amounts of individual lymphokines produced. More clones produced multiple lymphokines than would be expected from independent control. Taken together, this pattern of regulation is consistent with the hypothesis that antigen stimulation of T cells results in the activation of all the lymphokine genes, but the amount of each produced is determined by secondary controlling mechanisms.

摘要

总共对233个原发性同种异体反应性T细胞克隆进行了检测,以确定它们是否产生白细胞介素-2(IL-2)、白细胞介素-3(IL-3)、免疫(γ)干扰素(IFN)、粒细胞-巨噬细胞集落刺激因子(CSF-2)、B细胞生长因子I和II(BCGFI、BCGFII)以及嗜酸性粒细胞分化因子(EDF)。通过嗜酸性粒细胞分化试验(EDA)对EDF进行检测。观察到两个主要的相关性:在用于检测CSF-2的骨髓增殖试验(BMPA)中,IL-3被证明是检测到的主要淋巴因子,并且EDA与BCGFII之间存在高度相关性。随后的研究表明,后一种相关性是因为单一因子负责这两种活性。除了这两个例外情况,以及可能由于不同检测方法检测到不止一种淋巴因子而导致的低水平相关性外,没有证据表明淋巴因子存在协同表达。所产生的单个淋巴因子的量存在很大差异。产生多种淋巴因子的克隆比独立对照预期的要多。总体而言,这种调节模式与以下假设一致,即T细胞的抗原刺激导致所有淋巴因子基因的激活,但每种淋巴因子的产生量由二级控制机制决定。

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