FeatureImmunology · Autoimmunity
The Splicing Factor That Safeguards the T Cell
How a T cell specific deletion of CLNS1A reveals a previously unrecognized control point for genome stability, cell cycle progression, and the boundary between healthy immunity and autoimmunity.
Citation
Wang L, Noyer L, Jishage M, Wang YH, Tao AY, McDermott M, et al. CLNS1A regulates genome stability and cell cycle progression to control CD4 T cell function and autoimmunity. Sci Immunol. 2025;10(108):eadq8860.
Read on PubMed →The Model
Tissue specific conditional knockout, Cre driven, C57BL/6.
Explore Conditional Knockout ModelsModel Type
Conditional knockout (T cell specific deletion)
Target Gene
Clns1a (orthologous to human CLNS1A)
Strategy
Floxed Clns1a allele crossed to CD4-Cre to restrict deletion to CD4 T cells while preserving expression in other lineages
Background
C57BL/6
Validation
Deletion confirmed at the protein level in sorted CD4 T cells; litter matched controls used in all comparisons (verify specifics from Methods)
Therapeutic Area
Autoimmunity, T cell biology, genome stability
The Feske Lab
Stefan Feske, MD is Professor of Pathology at NYU Grossman School of Medicine. The Feske lab studies calcium signaling, gene expression, and cell cycle control in T cells, with a translational focus on primary immunodeficiency and autoimmune disease.
Published In
Science Immunology, 2026
Funding
NIH NIAID, plus additional support (full funding to be confirmed from paper).