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- Title
IFN-γ Regulates Murine Interferon-Inducible T Cell Alpha Chemokine (I-TAC) Expression in Dendritic Cell Lines and during Experimental Autoimmune Encephalomyelitis (EAE).
- Authors
Hamilton, N; Banyer, J; Hapel, A; Mahalingam, S; Ramsay, A; Ramshaw, I; Thomson, S
- Abstract
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)-γ 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-γ-receptor knockout (IFN-γR-/- ) 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-γR-/- 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.
- Publication
Scandinavian Journal of Immunology, 2002, Vol 55, Issue 2, p171
- ISSN
0300-9475
- Publication type
Academic Journal
- DOI
10.1046/j.1365-3083.1997.d01-93.x