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白细胞介素-4与γ干扰素在诱导正常人角质形成细胞细胞间黏附分子-1及主要组织相容性复合体II类抗原表达中的相互作用

Interleukin-4 and interferon-gamma interactions in the induction of intercellular adhesion molecule-1 and major histocompatibility complex class II antigen expression of normal human keratinocytes.

作者信息

Viac J, Gueniche A, Gatto H, Lizard G, Schmitt D

机构信息

INSERM U 346, Peau Humaine et Immunité, Clinique Dermatologique, Hôpital E Herriot, Lyon, France.

出版信息

Exp Dermatol. 1994 Apr;3(2):72-7. doi: 10.1111/j.1600-0625.1994.tb00050.x.

Abstract

Interleukin-4 (IL-4) that may be produced by T-helper cells in atopic lesions has immunomodulatory activities on skin cells which are poorly known. Our study was aimed at determining whether the cytokine exerts some effects on keratinocyte activation and can either enhance or antagonize interferon-gamma (IFN-gamma)-induced ICAM-1 or HLA-DR antigen expression. Using normal keratinocytes cultured in defined medium and cytofluorography, we showed that treatments of the human cells with the cytokine IL-4 alone had no effect on the induction of ICAM-1 or HLA-DR molecules. However, a transient, but significant enhanced expression of ICAM-1 was observed by the combination of IFN-gamma and IL-4 after 24 h of stimulation, which was followed by a reduction at 48 and 72 h. Conversely, IL-4, when added during the IFN-gamma activation stage, had no effect on MHC class II antigen expression of keratinocytes; however, the cytokine reduced the expression of these antigens when added 24 h before the stimulation by IFN-gamma. These results suggest that IFN-gamma and IL-4 may interact to regulate ICAM-1 and HLA-DR expression on keratinocytes.

摘要

特应性皮损中的辅助性T细胞可能产生的白细胞介素-4(IL-4)对皮肤细胞具有免疫调节活性,而这方面人们了解甚少。我们的研究旨在确定该细胞因子是否对角质形成细胞的激活有某些作用,以及它是增强还是拮抗干扰素-γ(IFN-γ)诱导的细胞间黏附分子-1(ICAM-1)或人类白细胞抗原-DR(HLA-DR)抗原表达。使用在限定培养基中培养的正常角质形成细胞和细胞荧光术,我们发现单独用细胞因子IL-4处理人细胞对ICAM-1或HLA-DR分子的诱导没有影响。然而,在刺激24小时后,IFN-γ和IL-4联合处理可观察到ICAM-1有短暂但显著的表达增强,随后在48小时和72小时表达下降。相反,在IFN-γ激活阶段添加IL-4对角质形成细胞的MHC II类抗原表达没有影响;然而,在IFN-γ刺激前24小时添加该细胞因子会降低这些抗原的表达。这些结果表明,IFN-γ和IL-4可能相互作用来调节角质形成细胞上ICAM-1和HLA-DR的表达。

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