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Published in: Cellular and Molecular Life Sciences, 2015, pp.DOI 10.1007/s00018-015-1873-7. ⟨10.1007/s00018-015-1873-7⟩

Authors: Stéphanie O Morin, Valentin Giroux, Cédric Favre, Yassina Bechah, Nathalie Auphan-Anezin, Romain Roncagalli, Jean-Louis Mege, Daniel Olive, Marie Malissen, Jacques A Nunes

Summary

The CD28 costimulatory receptor has a pivotal role in T cell biology as this molecule amplifies T cell receptor (TCR) signals to provide an efficient immune T cell response. There is a large debate about how CD28 mediates these signals. Here, we designed a CD28 gene targeted knock-in mouse strain lacking the cytoplasmic tail of CD28. As is the case in CD28-deficient (CD28 knockout) mice, regulatory T cell homeostasis and T cell activation are altered in these CD28 knock-in mice. Unexpectedly, the presence of a CD28 molecule deprived of its cytoplasmic tail could partially induce some early activation events in T cells such as signaling events or expression of early activation markers. These results unravel a new mechanism of T cell costimulation by CD28, independent of its cytoplasmic tail.

Link to Pubmed [PMID] – 25725801

Link to HAL – inserm-01122788

Link to DOI – 10.1007/s00018-015-1873-7