RT info:eu-repo/semantics/article
T1 Protein Kinase C η Is Required for T Cell Activation and Homeostatic Proliferation
A1 Fu, Guo
A1 Hu, Jianfang
A1 Niederberger-Magnenat, Nathalie
A1 Rybakin, Vasily
A1 Casas, Javier
A1 Yachi, Pia P.
A1 Feldstein, Stephanie
A1 Ma, Bo
A1 Hoerter, John A. H.
A1 Ampudia, Jeanette
A1 Rigaud, Stephanie
A1 Lambolez, Florence
A1 Gavin, Amanda L.
A1 Sauer, Karsten
A1 Cheroutre, Hilde
A1 Gascoigne, Nicholas R. J.
AB Protein kinase C η (PKCη) is abundant in T cells and is recruited to the immunological synapse that is formed between a T cell and an antigen-presenting cell; however, its function in T cells is unknown. We showed that PKCη was required for the activation of mature CD8+ T cells through the T cell receptor. Compared with wild-type T cells, PKCη-/- T cells showed poor proliferation in response to antigen stimulation, a trait shared with T cells deficient in PKCθ, which is the most abundant PKC isoform in T cells and was thought to be the only PKC isoform with a specific role in T cell activation. In contrast, only PKCη-deficient T cells showed defective homeostatic proliferation, which requires self-antigen recognition. PKCη was dispensable for thymocyte development; however, thymocytes from mice doubly deficient in PKCη and PKCθ exhibited poor development, indicating some redundancy between the PKC isoforms. Deficiency in PKCη or PKCθ had opposing effects on the relative numbers of CD4+ and CD8+ T cells. PKCη-/- mice had a higher ratio of CD4+ to CD8+ T cells compared to that of wild-type mice, whereas PKCθ-/- mice had a lower ratio. Mice deficient in both isoforms exhibited normal cell ratios. Together, these data suggest that PKCη shares some redundant roles with PKCθ in T cell biology and also performs nonredundant functions that are required for T cell homeostasis and activation.
SN 1945-0877
YR 2011
FD 2011
LK https://uvadoc.uva.es/handle/10324/64297
UL https://uvadoc.uva.es/handle/10324/64297
LA eng
NO Science signaling 4, ra84–ra84 (2011).
NO Producción Científica
DS UVaDOC
RD 02-dic-2024