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Cutting Edge |
,
,¶
*
Cancer Biology Program, Hematology/Oncology, Beth Israel-Deaconess Medical Center,
Bone Marrow Transplant Program,
Harvard Skin Disease Research Center, Harvard Medical School, Boston, MA 02115;
Bone Marrow Transplant Program, Department of Medicine, Massachusetts General Hospital, Boston, MA 02114; and
¶ Departments of Dermatology and Medicine, Brigham & Women’s Hospital, Boston, MA 02115
Murine bone marrow (BM) NK T cells can suppress
graft-vs-host disease, transplant rejection, and MLRs. Human BM
contains T cells with similar potential. Human BM was enriched for NK T
cells, 
50% of which recognized the nonpolymorphic CD1d molecule. In
contrast to the well-characterized blood-derived CD1d-reactive
invariant NK T cells, the majority of human BM CD1d-reactive T cells
used diverse TCR. Healthy donor invariant NK T cells rapidly produce
large amounts of IL-4 and IFN-
and can influence Th1/Th2
decision-making. Healthy donor BM CD1d-reactive T cells were Th2-biased
and suppressed MLR and, unlike the former, responded preferentially to
CD1d+ lymphoid cells. These results identify a novel
population of human T cells which may contribute to B cell development
and/or maintain Th2 bias against autoimmune T cell responses against
new B cell Ag receptors. Distinct CD1d-reactive T cell populations have
the potential to suppress graft-vs-host disease and stimulate antitumor
responses.
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