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人重组干扰素-β通过调节细胞因子分泌模式和归巢受体表达来影响辅助性T细胞亚群分化。

Human recombinant interferon-beta influences T helper subset differentiation by regulating cytokine secretion pattern and expression of homing receptors.

作者信息

McRae B L, Picker L J, van Seventer G A

机构信息

Department of Pathology, Division of Biological Sciences, University of Chicago, IL 60637-1463, USA.

出版信息

Eur J Immunol. 1997 Oct;27(10):2650-6. doi: 10.1002/eji.1830271026.

DOI:10.1002/eji.1830271026
PMID:9368622
Abstract

Type I interferons (IFN) are important regulators of both innate and acquired immunity. We have used an in vitro system of human CD4+ T cell differentiation to determine how IFN-beta influences development of T helper (Th) subsets and homing receptor expression. IFN-beta promoted differentiation of CD4+ T cells that produce low levels of both IFN-gamma and lymphotoxin compared to interleukin (IL)-12-derived Th1 CD4+ T cells. IFN-beta inhibited production of Th2 cytokines (IL-5 and IL-13) and augmented IL-12-mediated IL-10 secretion. In addition, IFN-beta significantly enhanced L-selection expression on CD4+ T cells and synergized with IL-12 to induce expression of cutaneous lymphocyte-associated antigen (CLA). This Th1 L-selectin+, CLA+ phenotype is characteristic of T cells found in normal human skin and suggests a role for type I IFN in the regulation of Th subset differentiation and tissue-specific homing receptors.

摘要

I型干扰素(IFN)是先天性免疫和获得性免疫的重要调节因子。我们利用人CD4+T细胞分化的体外系统来确定IFN-β如何影响辅助性T(Th)亚群的发育和归巢受体表达。与白细胞介素(IL)-12诱导的Th1 CD4+T细胞相比,IFN-β促进了产生低水平IFN-γ和淋巴毒素的CD4+T细胞的分化。IFN-β抑制Th2细胞因子(IL-5和IL-13)的产生,并增强IL-12介导的IL-10分泌。此外,IFN-β显著增强CD4+T细胞上L-选择素的表达,并与IL-12协同诱导皮肤淋巴细胞相关抗原(CLA)的表达。这种Th1 L-选择素阳性、CLA阳性的表型是正常人皮肤中T细胞的特征,提示I型干扰素在Th亚群分化和组织特异性归巢受体的调节中发挥作用。

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