Single-cell transcriptomics reveals targeted modulation of inflammatory repertoire by SOCE blockers
Store-operated calcium entry (SOCE) plays a critical role in regulating intracellular calcium signaling and is essential for immune cell functions. SOCE blockade with the pyrazole derivative BTP2 has been explored as an anti-inflammatory strategy in preclinical models, and Zegocractin (CM4620) is under clinical investigation as a CRAC channel inhibitor with activity in multiple tissues, including immune cells. However, the cell type-specific consequences of SOCE blockade under defined activation contexts remain incompletely understood. Here, we used multiplexed single-cell RNA sequencing to investigate the effects of two prototypic SOCE blockers, BTP2 and CM4620, on polyclonally stimulated, normal human peripheral blood mononuclear cells (PBMCs) in a phytohemagglutinin (PHA)-driven T-cell activation model. The data revealed that SOCE blockade suppressed cytotoxicity-associated transcriptional programs in CD8<sup>+</sup> effector T cells and natural killer (NK) cells, restoring them to levels comparable to unstimulated cells. At the same time, SOCE blockade allowed CD4<sup>+</sup> regulatory T cells to retain transcriptional signatures associated with immune regulation. These results indicate that, in this experimental model, SOCE blockade dampens cytotoxic programs while maintaining tolerance signatures, suggesting a potential avenue for targeted immune modulation in transplantation and other immune-mediated conditions. SIGNIFICANCE STATEMENT: Store-operated calcium entry (SOCE) is essential for immune activation, but broad immunosuppression can cause significant side effects. Using single-cell transcriptomics in a phytohemagglutinin (PHA)-driven T-cell activation model, we show that SOCE blockade with BTP2 or CM4620 suppresses pro-inflammatory and cytotoxic programs in CD8<sup>+</sup> effector T cells and NK cells while preserving tolerance-associated pathways in CD4<sup>+</sup> regulatory T cells. These findings suggest that SOCE blockade may provide a more targeted form of immune modulation, warranting future head-to-head comparisons with conventional immunosuppressants. Our results highlight the potential of SOCE blockers to reduce immune-mediated damage while maintaining tolerance, motivating further functional and translational studies in transplantation and other immune-mediated conditions.
Authors
- Chendong Pan (ORCID: https://orcid.org/0000-0003-3058-7247)
- Thangamani Muthukumar (ORCID: https://orcid.org/0000-0002-0294-6209)
- Divya Shankaranarayanan (ORCID: https://orcid.org/0009-0006-8028-9618)
- Iwijn De Vlaminck (ORCID: https://orcid.org/0000-0001-6085-7311)
- Mila Lagman
- Andreas Stephanou
- Carol Li
- Madhav Mantri
- Yanjie Sun
- Khaled Machaca
- Manikkam Suthanthiran
- Jenny Xiang
Institutions
- George Washington University (US)
- Cornell University (US)
- Presbyterian Hospital (US)
- Washington University Medical Center (US)
- New York Genome Center (US)
- Weill Cornell Medicine (US)
Publication Details
- Journal
- Human Immunology
- Published
- 2026-02-13
- DOI
- https://doi.org/10.1016/j.humimm.2026.111687
- Primary Topic
- Ion Channels and Receptors
- Type
- article
- Field-Weighted Citation Impact
- 0.00