IGIF并不驱动Th1细胞的发育，但可与IL-12协同作用以产生γ干扰素，并激活IRAK和核因子κB。

IGIF does not drive Th1 development but synergizes with IL-12 for interferon-gamma production and activates IRAK and NFkappaB.

作者信息

Robinson D, Shibuya K, Mui A, Zonin F, Murphy E, Sana T, Hartley S B, Menon S, Kastelein R, Bazan F, O'Garra A

机构信息

Department of Immunobiology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, California 94304, USA.

出版信息

Immunity. 1997 Oct;7(4):571-81. doi: 10.1016/s1074-7613(00)80378-7.

DOI:10.1016/s1074-7613(00)80378-7

PMID:9354477

Abstract

In these studies, IFN gamma-inducing factor (IGIF), unlike IL-12, did not drive Th1 development in BALB/c or C57BL/6 mice, but like IL-1alpha, potentiated IL-12-driven Th1 development in BALB/c mice. IGIF and IL-12 synergized for IFN gamma production from Th1 cells. Unlike IL-1alpha, IGIF had no effect on Th2 cells. IGIF signaled through IRAK, IL-1 receptor-associated kinase, to induce nuclear translocation of p65/p50 NFkappaB in Th1 cells. IL-1alpha had no effect on proliferation, cytokine production, or NFkappaB activation in Th1 cells but activated NFkappaB and proliferation in Th2 cells. Thus, Th1 and Th2 cells may differ in responsiveness and receptor expression for IL-1 family molecules. IGIF and IL-1alpha may differentially amplify Th1 and Th2 effector responses, respectively.

摘要

在这些研究中，与白细胞介素-12（IL-12）不同，干扰素γ诱导因子（IGIF）不会在BALB/c或C57BL/6小鼠中驱动Th1细胞发育，但与白细胞介素-1α（IL-1α）一样，能增强IL-12驱动的BALB/c小鼠Th1细胞发育。IGIF和IL-12协同促进Th1细胞产生干扰素γ。与IL-1α不同，IGIF对Th2细胞没有影响。IGIF通过白细胞介素-1受体相关激酶（IRAK）发出信号，诱导Th1细胞中p65/p50核因子κB（NFκB）的核转位。IL-1α对Th1细胞的增殖、细胞因子产生或NFκB激活没有影响，但能激活Th2细胞中的NFκB并促进其增殖。因此，Th1和Th2细胞对IL-1家族分子的反应性和受体表达可能存在差异。IGIF和IL-1α可能分别以不同方式放大Th1和Th2效应反应。