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*
Immunobiology Section, Yale University School of Medicine, New Haven, CT 06510;
Cancer Biology Program, Division of Hematology/Oncology, Beth Israel Deaconess Medical Center, Boston, MA 02215;
Gastrointestinal Unit (Medical Services), Massachusetts General Hospital, Boston, MA 02116; and
Department of Molecular Immunology, Graduate School of Medicine, Chiba University, Chuoku Chiba, Japan
During peripheral T cell deletion, lymphocytes accumulate in
nonlymphoid organs including the liver, a tissue that expresses the
nonclassical, MHC-like molecule, CD1. Injection of anti-CD3 Ab
results in T cell activation, which in normal mice is followed by
peripheral T cell deletion. However, in CD1-deficient mice, the
deletion of the activated T cells from the lymph nodes was impaired.
This defect in peripheral T cell deletion was accompanied by attenuated
accumulation of CD8+ T cells in the liver. In
tetra-parental bone marrow chimeras, expression of CD1 on the T cells
themselves was not required for T cell deletion, suggesting a role for
CD1 on other cells with which the T cells interact. We tested whether
this role was dependent on the Ag receptor-invariant, CD1-reactive
subset of NK T cells using two other mutant mouse lines that lack most
NK T cells, due to deletion of the genes encoding either
2-microglobulin or the TCR element J
281. However,
these mice had no abnormality of peripheral T cell deletion. These
findings indicate a novel role for CD1 in T cell deletion, and show
that CD1 functions in this process through mechanisms that does not
involve the major, TCR-invariant set of NK T
cells.
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