IFN-gamma regulates murine interferon-inducible T cell alpha chemokine (I-TAC) expression in dendritic cell lines and during experimental autoimmune encephalomyelitis (EAE).
IFN-gamma regulates murine interferon-inducible T cell alpha chemokine (I-TAC) expression in dendritic cell lines and during experimental autoimmune encephalomyelitis (EAE).
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IFN-gamma 调节树突状细胞系中和实验性自身免疫性脑脊髓炎 (EAE) 期间的鼠干扰素诱导 T 细胞 α 趋化因子 (I-TAC) 表达。
DOI:
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发表时间:
2002
影响因子:
3.7
通讯作者:
Scott Thomson
中科院分区:
文献类型:
--
作者:
N. H. R. Hamilton;J. Banyer;A. Hapel;S. Mahalingam;Alistair J. Ramsay;I. Ramshaw;Scott Thomson
Murine interferon-inducible T cell alpha chemokine (I-TAC) is a potent non-ELR Cys-X-Cys (CXC) chemokine that predominantly attracts activated T lymphocytes and binds to the receptor CXCR3. Using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) we analysed murine I-TAC expression in two different progenitor dendritic cell (DC) lines, MTHC-D2 and JAWS II which were exposed to various cytokines, and Con A-activated splenocytes from a panel of knockout mice. Analysis of the progenitor DC lines and Con A cultures demonstrated that murine I-TAC is primarily regulated by interferon (IFN)-gamma via interferon regulatory factor (IRF)-1. It has been proposed that I-TAC may have a role in autoimmune diseases such as multiple sclerosis (MS). Because I-TAC appears to be secreted from antigen-presenting cells (APCs) and attracts activated T cells, we examined the level of murine I-TAC mRNA in the central nervous system (CNS) of wild-type and IFN-gamma-receptor knockout (IFN-gammaR-/-) mice with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide-induced experimental autoimmune encephalomyelitis (EAE). Peak I-TAC expression was detected in wild-type mice on day 14 when the mice begin to recover, whereas very low levels of I-TAC were detected in the CNS of IFN-gammaR-/- mice which develop severe EAE and die. The expression characteristics of murine I-TAC suggest an important mediator of immune cell communication that could augment vaccines and autoimmune therapies.
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影响因子:
15.9
作者:
Mach, F;Sauty, A;Luster, AD
通讯作者:
Luster, AD
影响因子:
56.9
作者:
HUANG, S;HENDRIKS, W;AGUET, M
通讯作者:
AGUET, M
影响因子:
4.4
作者:
S. Gasperini;M. Marchi;F. Calzetti;Carlo Laudanna;L. Vicentini;Henrik S. Olsen;Marianne Murphy;Fang Liao;Joshua M. Farber;M. Cassatella
通讯作者:
S. Gasperini;M. Marchi;F. Calzetti;Carlo Laudanna;L. Vicentini;Henrik S. Olsen;Marianne Murphy;Fang Liao;Joshua M. Farber;M. Cassatella
影响因子:
4.4
作者:
Alain Sauty;Michelle Dziejman;R. Taha;Albert S. Iarossi;K. Neote;Eduardo A. Garcia-Zepeda;Qutayba A. Hamid;Andrew D. Luster
通讯作者:
Alain Sauty;Michelle Dziejman;R. Taha;Albert S. Iarossi;K. Neote;Eduardo A. Garcia-Zepeda;Qutayba A. Hamid;Andrew D. Luster
DOI:
--
发表时间:
1993
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Hulkower,K;Brosnan,CF;Aquino,DA;Cammer,W;Kulshrestha,S;Guida,MP;Rapoport,DA;Berman,JW
通讯作者:
Berman,JW