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Original Article

Department of Microbiology and Immunology, University of California at San Francisco, San Francisco CA 94143

Address correspondence to Nigel Killeen, Dept. of Microbiology and Immunology, University of California at San Francisco, San Francisco, CA 94143-0414. Phone: 415-502-5495; Fax: 415-502-8424; E-mail: nigel{at}itsa.ucsf.edu

Absence of CD4 impairs the efficiency of T cell receptor (TCR) signaling in response to major histocompatibility complex (MHC) class II–presented peptides. Here we use mice carrying a conditional Cd4 allele to study the consequences of impaired TCR signaling after the completion of thymocyte development. We show that loss of CD4 decreases the steady-state proliferation of T cells as monitored by in vivo labeling with bromo-deoxyuridine. Moreover, T cells lacking CD4 compete poorly with CD4-expressing T cells during proliferative expansion after transfer into lymphopenic recipients. The data suggest that T cells compete with one another during homeostatic proliferation, and indicate that the basis of this competition is TCR signaling.

Key Words: CD4 • T lymphocytes • helper • gene targeting • CD4-positive T lymphocytes

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