Temporal CRAC channel blockade modulates the MYC-MXD axis to attenuate autoimmune inflammation
(CRAC) channels for their effector function. Here, we demonstrate that Th17 cells are uniquely sensitive to temporal inhibition of CRAC channels. Temporal CRAC channel block disturbed the effector functions and metabolic programming of Th17 cells, which were rescued by MYC expression. We uncovered a regulatory hierarchy in which CRAC channel activity during differentiation maintains MYC function by repressing Mxd genes, which antagonize MYC. In an animal model of autoimmunity, temporal CRAC channel block increased MXD expression to attenuate Th17 pathogenicity. These observations extend to human Th17 cells, where temporal CRAC channel blockade also impacts the MYC-MXD axis to impede cytokine production. Collectively, our study identifies a role for CRAC channels in regulating the MYC-MXD balance that governs Th17 effector function.
Authors
- Yousang Gwack (ORCID: https://orcid.org/0000-0002-2821-9245)
- Reuben H. Kim (ORCID: https://orcid.org/0000-0001-5635-7728)
- Sonal Srikanth (ORCID: https://orcid.org/0000-0002-3034-095X)
- Beibei Wu (ORCID: https://orcid.org/0000-0002-0784-0745)
- Spyridon Hasiakos (ORCID: https://orcid.org/0000-0001-7477-9094)
- Zuoming Sun (ORCID: https://orcid.org/0000-0003-1896-6666)
- Matthew Do
- Shawn Cokus
- Matteo Pellegrini
- Elizabeth Kaplan
Institutions
- City Of Hope National Medical Center (US)
- University of California, Los Angeles (US)
- UCLA Health (US)
- City of Hope (US)
- Beckman Research Institute
Publication Details
- Journal
- Cell Reports
- Published
- 2026-09-16
- DOI
- https://doi.org/10.1016/j.celrep.2026.118017
- Primary Topic
- Ion Channels and Receptors
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Foundation for the National Institutes of Health