Single-cell transcriptomic signatures of T cells associated with rituximab responsiveness in idiopathic nephrotic syndrome.

Authors

Eri Koshi-Ito, Yu Watanabe, Chikao Onogi, Asuka Horinouchi, Koichi Ogami, Seiko Yoshino, Yohei Sugimoto, Shintaro Komatsu, Akihito Tanaka, Kazuhiro Furuhashi, Shoichi Maruyama, Hiroshi I Suzuki

Published in

iScience. Volume 29. Issue 9. Pages 117237. Sep 18, 2026. Epub Aug 24, 2026.

Abstract

Rituximab (RTX) is increasingly used in steroid-dependent minimal change disease, a leading cause of idiopathic nephrotic syndrome (INS), yet predictors of response remain unclear. Although RTX primarily targets B cells, T cells are also implicated in INS pathogenesis. We investigated RTX-induced T cell dynamics by single-cell RNA sequencing/T cell receptor profiling of peripheral T cells from three responders and three non-responders before and after RTX treatment. Responders exhibited RTX-driven broad transcriptomic remodeling, accompanied by reduced exhausted CD8⁺ T cells and clonal expansion of CD4⁺ cytotoxic T cells with enhanced oxidative phosphorylation (OXPHOS) signatures, whereas non-responders showed marginal changes. In a separate cohort, reactive oxygen species (ROS) levels tended to be higher in responders, and declined post-RTX, collectively associating enhanced mitochondrial activity with favorable response. Reanalysis of childhood INS data supported altered B-T cell crosstalk and T cell metabolism. Together, T cells may influence RTX responsiveness, warranting further biomarker studies.

PMID:
42668630
Bibliographic data and abstract were imported from PubMed on 30 Aug 2026.

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