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-Dependent Mechanism
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* Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115;
Department of Applied Biological Chemistry, University of Tokyo, Tokyo, Japan; and
National Food Research Institute, Tsukuba, Ibaraki, Japan
Murine CD4+CD25+ regulatory cells have been reported to express latency-associated peptide (LAP) and TGF-
on the surface after activation, and exert regulatory function by the membrane-bound TGF- in vitro. We have now found that a small population of CD4+ T cells, both CD25+ and CD25-, can be stained with a goat anti-LAP polyclonal Ab without being stimulated. Virtually all these LAP+ cells are also positive for thrombospondin, which has the ability to convert latent TGF- to the active form. In the CD4+CD45RBhigh-induced colitis model of SCID mice, regulatory activity was exhibited not only by CD25+LAP+ and CD25+LAP- cells, but also by CD25-LAP+ cells. CD4+CD25-LAP+ T cells were part of the CD45RBlow cell fraction. CD4+CD25-LAP-CD45RBlow cells had minimal, if any, regulatory activity in the colitis model. The regulatory function of CD25-LAP+ cells was abrogated in vivo by anti-TGF- mAb. These results identify a new TGF--dependent regulatory CD4+ T cell phenotype that is CD25- and LAP+.
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