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Updated: Aug 31, 2026
Assessment of Human Natural Killer Cell Events Driven by FcγRIIIa Engagement in the Presence of Therapeutic Antibodies
Published on: May 22, 2020
Single-cell transcriptomic signatures of T cells associated with rituximab responsiveness in idiopathic nephrotic
Eri Koshi-Ito1,2, Yu Watanabe1,3, Chikao Onogi1
1Department of Nephrology, Internal Medicine, Graduate School of Medicine, Nagoya University, Nagoya 466-8550, Japan.
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.
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.