
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.
CD4-Positive T-Lymphocytes, Male, Receptors, Antigen, T-Cell, Cell Differentiation, Mice, Transgenic, Major Histocompatibility Complex, Mice, Inbred C57BL, Mice, CD4 Antigens, Mutation, Animals, Humans, Female, Signal Transduction
CD4-Positive T-Lymphocytes, Male, Receptors, Antigen, T-Cell, Cell Differentiation, Mice, Transgenic, Major Histocompatibility Complex, Mice, Inbred C57BL, Mice, CD4 Antigens, Mutation, Animals, Humans, Female, Signal Transduction
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