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24JQ T Cells: A Feedback Mechanism for Immune Regulation1
*
Division of Infectious Diseases, University of California Medical Center, Los Angeles, CA 90095;
AIDS Research Center/Infectious Disease Unit, Massachusetts General Hospital-East, Charlestown, MA 02129;
Cancer Immunology and AIDS, Dana Farber Cancer Institute, Boston, MA 02115;
§
Genetics Institute, Cambridge, MA 02140;
¶
Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138; and
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Department of Pathology, Johns Hopkins University, Baltimore, MD 21287
The precise immunologic functions of CD1d-restricted,
CD161+ AV24AJ18 (V
24JQ) T cells are not well defined,
although production of IL-4 has been suggested as important for priming
Th2 responses. However, activation of human V24JQ T cell clones
by anti-CD3 resulted in the secretion of multiple cytokines notably
important for the recruitment and differentiation of myeloid dendritic
cells. Specific activation of V24JQ T cells was CD1d restricted.
Expression of CD1d was found on monocyte-derived dendritic cells in
vitro, and immunohistochemical staining directly revealed CD1d
preferentially expressed on dendritic cells in the paracortical T cell
zones of lymph nodes. Moreover, myeloid dendritic cells both activated
V24JQ T cells and were susceptible to lysis by these same
regulatory T cells. Because myeloid dendritic cells are a major source
of IL-12 and control Th1 cell differentiation, their elimination by
lysis is a mechanism for limiting the generation of Th1 cells and thus
regulating Th1/Th2 responses.
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