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-Induced Secretion of C-C Chemokines Modulates C-C Chemokine Receptor 5 Expression on Peripheral Blood Lymphocytes
*
Laboratory of Immunology and
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
Peripheral blood lymphocytes express CCR5, a chemokine receptor for
immune cell migration and calcium signaling that serves as an important
coreceptor for the HIV. After in vitro stimulation, CCR5 expression is
dramatically increased on mature T lymphocytes, especially on the
CD45RO+ memory subset. In this study, we report that
TNF-
delays the surface expression of CCR5 on PBLs after activation
and diminishes CCR5 irrespective of its initial level. Functional loss
of CCR5 is reflected in a decreased capability of the treated cells to
migrate and signal calcium after MIP-1ß stimulation. The effect is
mediated via the p80 type II TNF receptor (TNFR2), which induces
NF-
B among other factors, leading to an enhanced secretion of the
chemokines macrophage-inflammatory protein-1,
macrophage-inflammatory protein-1ß, and RANTES. Expression of these
chemokines directly down-regulates CCR5. These findings reveal a new
regulatory mechanism utilized by activated peripheral T cells to
modulate their chemotaxis and potentially other functions mediated by
CCR5, including the infection of T lymphocytes by macrophage-tropic HIV
strains.
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