STAP-2 Is a Novel Positive Regulator of TCR-Proximal Signals.


Journal

Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R

Informations de publication

Date de publication:
01 07 2022
Historique:
received: 22 10 2021
accepted: 19 04 2022
pubmed: 21 6 2022
medline: 2 7 2022
entrez: 20 6 2022
Statut: ppublish

Résumé

TCR ligation with an Ag presented on MHC molecules promotes T cell activation, leading to the selection, differentiation, and proliferation of T cells and cytokine production. These immunological events are optimally arranged to provide appropriate responses against a variety of pathogens. We here propose signal-transducing adaptor protein-2 (STAP-2) as a new positive regulator of TCR signaling. STAP-2-deficient T cells showed reduced, whereas STAP-2-overexpressing T cells showed enhanced, TCR-mediated signaling and downstream IL-2 production. For the mechanisms, STAP-2 associated with TCR-proximal CD3ζ immunoreceptor tyrosine activation motifs and phosphorylated LCK, resulting in enhancement of their binding after TCR stimulation. In parallel, STAP-2 expression is required for full activation of downstream TCR signaling. Importantly, STAP-2-deficient mice exhibited slight phenotypes of CD4

Identifiants

pubmed: 35725273
pii: jimmunol.2101014
doi: 10.4049/jimmunol.2101014
doi:

Substances chimiques

Adaptor Proteins, Signal Transducing 0
Receptors, Antigen, T-Cell 0
STAP2 protein, mouse 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

57-68

Informations de copyright

Copyright © 2022 by The American Association of Immunologists, Inc.

Auteurs

Kodai Saitoh (K)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Jun-Ichi Kashiwakura (JI)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Kota Kagohashi (K)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Yuto Sasaki (Y)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Shoya Kawahara (S)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Yuichi Sekine (Y)

Department of Cell Biology, Kyoto Pharmaceutical University, Kyoto, Japan.

Yuichi Kitai (Y)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Ryuta Muromoto (R)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Michiko Ichii (M)

Department of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Hiroko Nakatsukasa (H)

Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-Ku, Tokyo, Japan; and.

Akihiko Yoshimura (A)

Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-Ku, Tokyo, Japan; and.

Kenji Oritani (K)

Department of Hematology, International University of Health and Welfare, Narita, Chiba, Japan.

Tadashi Matsuda (T)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan; tmatsuda@pharm.hokudai.ac.jp.

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Classifications MeSH