Kewei Ye
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Kewei Ye has a total of 22 co-authors. Here are the top co-authors by number of shared publications:
Amanda Borgenstam
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden
1 shared publication- Anatoly Dubnovitsky
Department of Medicine, Division of Rheumatology, Karolinska Institutet, and Center for Molecular Medicine (CMM), Karolinska University Hospital, Stockholm, Sweden
1 shared publication Anja Kramer
Division of Immunology and Respiratory Medicine, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden
1 shared publication- Ari Waisman
Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz
1 shared publication - Erik Benson
Science for Life Laboratory (SciLifeLab) Department of Microbiology Tumor and Cell Biology Karolinska Institutet Solna Sweden
1 shared publication Fanxi Meng
Division of Immunology and Respiratory Medicine, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden
1 shared publication
Latest Publications
- 16 July 2026
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 393 (6808) , eadx9264
Direct interaction of Vδ7 TCRs with IL17RA drives the differentiation of T H 1-like γδT cells
Of the three classes of lymphocytes that constitute the adaptive immune system, γδT cells are the only class for which the principles of antigen recognition remain enigmatic. Although endogenous γδT cell antigen receptor (γδTCR) ligands are thought to regulate γδT cell development, their identities are largely elusive. Here, we identified the interleukin 17 receptor A chain (IL17RA) as a γδTCR ligand that drove the differentiation of Vδ7 + γδT cells with a T helper 1 (T H 1)–like effector program in mice. IL17RA promoted this differentiation through an interaction involving germline-encoded regions of the Vδ7 chain, enabling the selection of cells with a diverse CDR3 repertoire and thus acting as a nonclonotypic γδTCR ligand. Together with the nonclonotypic mode of γδTCR engagement by butyrophilins, these results suggest that such interactions represent a general biological mechanism shaping the γδT cell compartment.
- 16 July 2026
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 393 (6808) , eadx9264
Direct interaction of Vδ7 TCRs with IL17RA drives the differentiation of T H 1-like γδT cells
Of the three classes of lymphocytes that constitute the adaptive immune system, γδT cells are the only class for which the principles of antigen recognition remain enigmatic. Although endogenous γδT cell antigen receptor (γδTCR) ligands are thought to regulate γδT cell development, their identities are largely elusive. Here, we identified the interleukin 17 receptor A chain (IL17RA) as a γδTCR ligand that drove the differentiation of Vδ7 + γδT cells with a T helper 1 (T H 1)–like effector program in mice. IL17RA promoted this differentiation through an interaction involving germline-encoded regions of the Vδ7 chain, enabling the selection of cells with a diverse CDR3 repertoire and thus acting as a nonclonotypic γδTCR ligand. Together with the nonclonotypic mode of γδTCR engagement by butyrophilins, these results suggest that such interactions represent a general biological mechanism shaping the γδT cell compartment.