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Original Article |
Correspondence to: Terri M. Laufer, 421 Curie Blvd., BRB II/III 753, University of Pennsylvania School of Medicine, Philadelphia, PA 19104. Tel:215-573-2955 Fax:215-573-7599 E-mail:tlaufer{at}mail.med.upenn.edu.
CD4+25+ T cells are a unique population of immunoregulatory T cells which are critical for the prevention of autoimmunity. To address the thymic selection of these cells we have used two models of attenuated thymic deletion. In K14-Aßb mice, major histocompatibility complex (MHC) class II I-Ab expression is limited to thymic cortical epithelium and deletion by hematopoietic antigen-presenting cells does not occur. In H2-DM
–deficient mice, MHC class II molecules contain a limited array of self-peptides resulting in inefficient clonal deletion. We find that CD4+25+ T cells are present in the thymus and periphery of K14-Aßb and H2-DM–deficient mice and, like their wild-type counterparts, suppress the proliferation of cocultured CD4+25- effector T cells. In contrast, CD4+25+ T cells from MHC class II–deficient mice do not suppress responder CD4+ T cells in vitro or in vivo. Thus, development of regulatory CD4+25+ T cells is dependent on MHC class II-positive thymic cortical epithelium. Furthermore, analysis of the specificities of CD4+25+ T cells in K14-Aßb and H2-DM–deficient mice suggests that a subset of CD4+25+ T cells is subject to negative selection on hematopoietic antigen-presenting cells.
Key Words:
autoimmune disease, self-tolerance, thymic development, IL-2 receptor chain (CD25), suppressor T cells
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