Sialic acids on T cells are crucial for their maintenance and survival.

Autor:	Schmidt M; Division of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany., Linder AT; Division of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany., Korn M; Division of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany., Schellenberg N; Division of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany., Meyer SJ; Division of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany., Nimmerjahn F; Division of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany., Werner A; Division of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany., Abeln M; Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany., Gerardy-Schahn R; Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany., Münster-Kühnel AK; Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany., Nitschke L; Division of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany.
Jazyk:	angličtina
Zdroj:	Frontiers in immunology [Front Immunol] 2024 Jun 14; Vol. 15, pp. 1359494. Date of Electronic Publication: 2024 Jun 14 (Print Publication: 2024).
DOI:	10.3389/fimmu.2024.1359494
Abstrakt:	Sialic acids are found as terminal sugars on glycan structures on cellular surfaces. T cells carry these sialoglycans abundantly, and they are thought to serve multiple functions in cell adhesion, cell migration, and protection from complement attack. We studied the role of sialoglycans on T cells in a mouse model with a T cell-specific deletion of cytidine monophosphate-sialic acid synthase (CMAS), the enzyme that is crucial for the synthesis of sialoglycans. These mice showed a T-cell deficiency in peripheral lymphoid organs. Many T cells with an undeleted Cmas allele were found in the periphery, suggesting that they escaped the Cre-mediated deletion. The remaining peripheral T cells of T cell-specific Cmas KO mice had a memory-like phenotype. Additional depletion of the complement factor C3 could not rescue the phenotype, showing that the T-cell defect was not caused by a host complement activity. Cmas -deficient T cells showed a high level of activated caspase 3, indicating an ongoing apoptosis. In bone marrow chimeric cellular transfer experiments, we observed a strong competitive disadvantage of Cmas -deficient T cells compared to wild-type T cells. These results show that sialoglycans on the surface of T cells are crucial for T-cell survival and maintenance. This function has not been recognized before and is similar to the function of sialoglycans on B cells. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision. (Copyright © 2024 Schmidt, Linder, Korn, Schellenberg, Meyer, Nimmerjahn, Werner, Abeln, Gerardy-Schahn, Münster-Kühnel and Nitschke.)
Databáze:	MEDLINE
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