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Proliferating CD4⁺ T Cells Undergo Immediate Growth Arrest upon Cessation of TCR Signaling In Vivo¹

Cory A. Yarke^*, Stacy L. Dalheimer^*, Na Zhang^*, Drew M. Catron, Marc K. Jenkins and Daniel L. Mueller^2,*

^* Department of Medicine and Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455

To investigate the role of TCR signaling in the exit of CD4⁺ T cells from cell cycle, we took advantage of a low frequency TEa T cell adoptive transfer technique as well as the Y-Ae mAb to interrupt Ag/MHC recognition before the completion of clonal expansion. Termination of TCR signaling after 36 h of Ag exposure caused an immediate reduction in cell size and deceleration of G₁—>SG₂M phase cell cycle progression. As a consequence, clonal expansion in the absence of durable TCR signaling decreased by two-thirds. Thus, CD4⁺ T cells scan for the presence Ag throughout their clonal expansion response, and continuously adjust their rate of cell growth and G₁—>S phase transition to match their intensity of TCR signaling.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by NIH P01 AI35296 (to D.L.M.) and an Immunology Training Grant T32 AI07313 (to C.A.Y.).

² Address correspondence and reprint requests to Dr. Daniel L. Mueller, Department of Medicine and Center for Immunology, University of Minnesota Medical School, MMC 334, 6-120 Nils Hasselmo Hall, 312 Church Street Southeast, Minneapolis, MN 55455. E-mail address: muell002{at}umn.edu

³ Abbreviations used in this paper: pE, I-E^d -chain peptide 52–68; FSC, forward scatter; TCR-Tg, TCR-transgenic; E RFP, E red fluorescent protein.