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-Inducible T Cell 
Chemoattractant Is a Potent Stimulator of Normal Human Blood T Lymphocyte Transendothelial Migration: Differential Regulation by IFN- and TNF-1
,
,
Departments of
* Pediatrics,
Medicine,
Microbiology/Immunology, and Pathology, Dalhousie University, Halifax, Nova Scotia, Canada
Previous studies have shown that the CXC chemokine,
IFN-
-inducible T cell 
chemoattractant (I-TAC), was chemotactic
for IL-2-activated human T lymphocytes, which express abundant CXCR3.
However, because most memory T lymphocytes are also CXCR3+,
the ability of I-TAC to promote the migration of normal human blood T
cells across HUVEC monolayers in Transwell chambers was examined. I-TAC
induced a marked (4- to 6-fold) increase in transendothelial migration
(TEM) of T cells across unstimulated HUVEC from 5.6 to 28% of input T
cells and was substantially more active than IFN--inducible
protein-10, another CXCR3 ligand. I-TAC significantly enhanced TEM of T
cells across TNF-, but not across IFN- or IFN- plus
TNF--activated HUVEC. IFN- or IFN- plus TNF--activated
HUVEC produced substantial amounts of I-TAC, in contrast to
TNF--treated EC. Both CD4+ and CD8+ T cells
migrated in response to I-TAC to a similar extent, while memory T cells
migrated several fold better than naive T cells. Blockade of LFA-1
strongly inhibited I-TAC-induced T cell TEM across unstimulated HUVEC,
and 
50–60% of the TEM across cytokine-activated HUVEC. However,
blocking both LFA-1 and very late Ag-4 abolished I-TAC induced T cell
TEM. In vivo significant levels of I-TAC were detected in arthritic
synovial fluid. Thus, I-TAC is one of the most potent chemoattractants
of normal human blood CD4 and CD8 T cell TEM and is likely a major
mediator of blood memory T lymphocyte migration to
inflammation.
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