Involvement of CD1 in peripheral deletion of T lymphocytes is independent of NK T cells

During peripheral T cell deletion, lymphocytes accumulate in nonlymphoid or gans including the liver, a tissue that expresses the nonclassical, MHC-lik e molecule, CD1. Injection of anti-CD3 Ab results in T cell activation, whi ch in normal mice is followed by peripheral T cell deletion. However, in CD 1-deficient mice, the deletion of the activated T cells from the lymph node s was impaired. This defect in peripheral T cell deletion was accompanied b y 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 tell with which the T cells interact. We tested whether this role was dependent on th e 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 beta (2)-microglobolin or the TCR element J alpha 281. Howe ver, these mice had no abnormality of peripheral T cell deletion. These fin dings indicate a novel role for CD1 in T cell deletion, and show that CD1 f unctions in this process through mechanisms that does not involve the major , TCR-invariant set of NK T cells.