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The Journal of Immunology, 2001, 167: 6706-6710.
Copyright © 2001 by The American Association of Immunologists


Cutting Edge

Cutting Edge: Regulation of CD8+ T Cell Proliferation by 2B4/CD48 Interactions1

Taku Kambayashi2,*, Erika Assarsson2,*, Benedict J. Chambers* and Hans-Gustaf Ljunggren3,*,{dagger}

* Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden; and {dagger} Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden

The biological function of 2B4, a CD48-binding molecule expressed on T cells with an activation/memory phenotype, is not clear. In this report, we demonstrate that proliferation of CD8+ T cells is regulated by 2B4. Proliferative responses of CD8+ T cells were significantly reduced by anti-2B4 Ab. The effects were not potentiated by anti-CD48 Ab, suggesting that the observed responses were driven by 2B4/CD48 interactions. Surprisingly, the 2B4/CD48-dependent proliferative responses were also observed in the absence of APCs. This suggests that 2B4/CD48 interactions can occur directly between T cells. Furthermore, when activated 2B4+CD8+ T cells were mixed with 2B4-CD8+ TCR-transgenic T cells and specific peptide-loaded APC, the proliferation of the latter T cells was inhibited by anti-2B4 Ab. Taken together, this suggests that 2B4 on activated/memory T cells serves as a ligand for CD48, and by its ability to interact with CD48 provides costimulatory-like function for neighboring T cells.




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