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Blood, Vol. 95 No. 1 (January 1), 2000:
pp. 39-47
Activation of C-C  -chemokines in human peripheral blood
  T cells by isopentenyl pyrophosphate and regulation by
cytokines
Barbara Cipriani,
Giovanna Borsellino,
Fabrizio Poccia,
Roberta Placido,
Daniela Tramonti,
Simona Bach,
Luca Battistini, and
Celia F. Brosnan
From the I.R.C.C.S., Santa Lucia, Laboratory of Neuroimmunology,
Rome, Italy; the Department of Biology, University of Rome, Tor
Vergata, Rome, Italy; the Department of Pathology, Albert Einstein
College of Medicine, Bronx, NY; and the International Center for AIDS
and Emerging Infection Research Center, L. Spallanzani Institute for
Infectious Disease, Rome, Italy.
Human   T lymphocytes respond to viral, bacterial, protozoal,
and tumoral antigens, but their precise function remains unknown. In
adults the major circulating T-cell subset expresses the V9V2 T-cell receptor and responds to protease-resistant
phosphorylated derivatives found in many pathogens. In this study we
show that activation of V2+ cells with the nonpeptidic
antigen isopentenyl pyrophosphate (IPP) rapidly induces (within 4-12 hours) the C-C chemokines MIP-1 , MIP-1 , and lymphotactin but not
MCP-1. The most robust response was obtained for MIP-1. IPP
induction of MIP-1 and MIP-1 was not affected by costimulation
with interleukin-4 (IL-4), IL-10, TGF-, or interferon- (INF-).
However, IL-12 significantly enhanced IPP-induced expression and
release of MIP-1 that was down-regulated by TGF- whereas the
induction of MIP-1 by IPP+IL-12 was refractory to cotreatment
with TGF indicating that these chemokines are differentially
regulated by these cytokines. V2+ T cells also
expressed a wide range of C-C chemokine receptors including CCR1, CCR5,
and CCR8, all of which were down-regulated following activation. We
conclude that V2+ cells can be rapidly induced by
components of bacterial cell walls to express high levels of
proinflammatory chemokines, supporting an important role for these
cells in the early stages of the inflammatory responses to many common
pathogens. (Blood. 2000, 95:39-47)
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