Takuya Ohtani
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Takuya Ohtani has a total of 36 co-authors. Here are the top co-authors by number of shared publications:
- Ahmed Alaswad
Centre for Individualised Infection Medicine and TWINCORE, joint ventures between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover, Germany
1 shared publication - Ajinkya Pattekar
Institute for Immunology & Immune Health (I3H), Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
1 shared publication - Amit Singh
Institute for Biomechanics, ETH Zürich, Zürich, Switzerland
1 shared publication - Bertram Bengsch
Department of Internal Medicine, Medical Center - University of Freiburg, Freiburg, Germany
1 shared publication - David Obwegs
Faculty of Biology, University of Freiburg, Freiburg, Germany
1 shared publication - E. John Wherry
Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia, USA
1 shared publication
Latest Publications
- 6 February 2026
- Published by American Association for the Advancement of Science (AAAS) in Science Immunology
- Vol. 11 (116) , eadx8474
Single-cell profiling reveals diverse γδ T cell subsets in ulcerative colitis
γδ T cells maintain intestinal immune homeostasis, but their contributions to human ulcerative colitis (UC) are poorly understood. We characterized γδ T cells in intestinal biopsies obtained from patients with UC and healthy donors using single-cell RNA sequencing, T cell receptor profiling, and mass cytometry. UC reduced CD103 + Vγ4Vδ1 + γδ intraepithelial lymphocytes (γδ IELs) and increased γδ T cell subsets with stemlike phenotypes expressing TCF-1 (T cell factor 1) and PD-1 (programmed cell death receptor 1) or effector-like phenotypes expressing granzyme B, perforin, and T-bet in the lamina propria. γδ T cell composition changes in UC correlated with decreased expression of epithelial BTNL3 and BTNL8 and increased BTN3A1 and BTN3A3 , suggesting altered recruitment and activation. Clinical improvement recovered γδ IELs and reduced inflammation-associated subsets. Inflammation-associated changes were observed in peripheral blood γδ T cells. Thus, distinct γδ T cell subsets in different niches exert protective or pathogenic functions in UC.
- 6 February 2026
- Published by American Association for the Advancement of Science (AAAS) in Science Immunology
- Vol. 11 (116) , eadx8474
Single-cell profiling reveals diverse γδ T cell subsets in ulcerative colitis
γδ T cells maintain intestinal immune homeostasis, but their contributions to human ulcerative colitis (UC) are poorly understood. We characterized γδ T cells in intestinal biopsies obtained from patients with UC and healthy donors using single-cell RNA sequencing, T cell receptor profiling, and mass cytometry. UC reduced CD103 + Vγ4Vδ1 + γδ intraepithelial lymphocytes (γδ IELs) and increased γδ T cell subsets with stemlike phenotypes expressing TCF-1 (T cell factor 1) and PD-1 (programmed cell death receptor 1) or effector-like phenotypes expressing granzyme B, perforin, and T-bet in the lamina propria. γδ T cell composition changes in UC correlated with decreased expression of epithelial BTNL3 and BTNL8 and increased BTN3A1 and BTN3A3 , suggesting altered recruitment and activation. Clinical improvement recovered γδ IELs and reduced inflammation-associated subsets. Inflammation-associated changes were observed in peripheral blood γδ T cells. Thus, distinct γδ T cell subsets in different niches exert protective or pathogenic functions in UC.