Scand J Immunol 2002 Feb;55(2):171-7
Hamilton NH, Banyer JL, Hapel AJ, Mahalingam S, Ramsay AJ, Ramshaw IA, Thomson SA.
John Curtin School of Medical Research (JCSMR), Australian National University, Canberra, Australian Capital Territory, Australia.
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.