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and IL-12 differentially regulate CC-chemokine secretion and CCR5 expression in human T lymphocytes
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* Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy;
Experimental Medicine Research Center, San Giovanni Battista Hospital, Turin, Italy;
AIDS Immunopathogenesis Unit, Dibit, San Raffaele Scientific Institute, Milan, Italy;
Laboratory of Human Genetics of Infectious Diseases, Neckér Medical School, Paris, France;
|| The Picower Institute for Medical Research, Manhasset, New York;
# Wistar Institute, Philadelphia, Pennsylvania; and
** Department of Pathology, University of Verona, Italy
Correspondence: Dr. Francesco Novelli, Dipartimento di Scienze Cliniche e Biologiche, Università di Torino, Ospedale San Luigi Gonzaga, 10043 Orbassano, Italy; E-mail: franco.novelli{at}unito.it
Interleukin (IL)-12, especially in the presence of neutralizing anti-IL-4 monoclonal antibodies, primed CD45RO- T clones for high CCL3/macrophage-inflammatory protein-1
(MIP-1) and CCL4/MIP-1ß levels. In CD4+ and CD8+ clones from two patients deficient for IL-12Rß1 (IL-12Rß1-/-), production of CCL3/MIP-1 and CCL4/MIP-1ß was defective. CD4+ clones from two patients deficient for interferon-
(IFN-) R1 (IFN-R1-/-) produced somewhat decreased CCL4/MIP-1ß levels. IL-12 failed to prime CD4+ or CD8+ healthy clones for high CCL5/regulated on activation, normal T expressed and secreted (RANTES) production, although its secretion was impaired in CD4+ clones from IL-12Rß1-/- and IFN-R1-/- patients. CCR5 surface expression was up-regulated in resting peripheral blood mononuclear cells and CD4+ clones from both kinds of patients, rendering them more susceptible to CCR5-dependent (R5) HIV-1 infection. Neutralization of IFN- increased CCR5 expression and decreased CC-chemokine secretion by CD4+ clones from healthy and IL-12Rß1-/- individuals, suggesting an IFN--dependent control of CCR5 expression. These data provide the first documented analysis of chemokine secretion and chemokine receptor expression on T cells from IL-12 and IFN- receptor-deficient patients and dissect the role of IL-12 and IFN- on inducing inflammatory chemokine secretion and down-regulating CCR5 expression in human T cells.
Key Words: chemokine receptor • cytokine receptors • AIDS
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