Journal
JOURNAL OF IMMUNOLOGY
Volume 164, Issue 10, Pages 5383-5388Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.164.10.5383
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Funding
- NIAID NIH HHS [R01AI40710] Funding Source: Medline
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IFN-inducible T cell alpha chemoattractant (I-TAC) is a recently discovered member of the CXC chemokine family. It is a potent T cell chemoattractant expressed by IFN-gamma-treated astrocytes, monocytes, keratinocytes, bronchial epithelial cells, and neutrophils. In this study, we show that I-TAG is also expressed by IFN-gamma-treated endothelial cells (EC), both at the mRNA and protein levels. Induction of the I-TAG message is rapid and sustained over 24 h, TNF-alpha does not induce I-TAC mRNA alone,,but does act synergistically with IFN-gamma, Blocking Abs to I-TAG, or to its receptor, CXCR3, reduce T cell adhesion to EC monolayers demonstrating that the expressed protein is functional. Finally, the expression of I-TAG by EC is resistant to the immunosuppressive drug cyclosporin A, suggesting that I-TAG may contribute to the chronic immune inflammation characteristic of graft arteriosclerosis.
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