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A Pool of Central Memory-Like CD4 T Cells Contains Effector Memory Precursors

J. Magarian Blander^*, Derek B. Sant’Angelo, Daniela Metz, Sang-Won Kim^*, Richard A. Flavell^*, Kim Bottomly^* and Charles A. Janeway, Jr.^1,*

^* Section of Immunobiology, Yale University School of Medicine and Howard Hughes Medical Institute, New Haven, CT 06520; and Laboratory of T Cell Immunobiology, Memorial Sloan-Ketttering Cancer Center, and Weil Graduate School of Medical Sciences of Cornell University, New York, NY 10021; and David Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, University of Rochester, Rochester, NY 14642

The L51S mutation in the D10.G4.1 TCR -chain reduces the affinity of the TCR to its ligand by affecting the interactions among the TCR, the -chain of I-A^k, and the bound peptide. We show that this mutation drives the generation of a pool of memory CD44^highCD62L^negCD45RB^neg CD4 TCR transgenic T cells. Their activation threshold is low, such that they proliferate in response to lower concentrations of agonist peptides than naive L51S CD4 T cells. Unlike effector memory CD4 T cells, however, they lack immediate effector function in response to TCR stimulation. These cells express IL-2R only after culture with specific peptide. Although they can be recovered from lymph nodes, the majority lack the expression of the lymph node homing receptor CCR7. When these cells receive a second TCR stimulation in vitro, they differentiate into potent Th2-like effector cells, producing high levels of IL-4 at doses of agonist peptide too low to stimulate cytokine release from similarly differentiated naive L51S CD4 T cells. Having these properties, the L51S TCR transgenic memory CD4 T cells cannot be classified as either strict central memory or effector memory, but, rather, as a pool of memory T cells containing effector memory precursors.

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