Dominik Drmic
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Dominik Drmic has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
- Anthony Tao
Department of Pathology, New York University Grossman School of Medicine, New York, NY 10016, USA
1 shared publication - Ikjot Sidhu
Department of Immunology and Immunotherapy, Precision Immunology Institute, Icahn School of Medicine at Mt Sinai, New York, USA
1 shared publication Ivan Gando
Department of Pathology, New York University Grossman School of Medicine, New York, NY, USA
1 shared publicationKatherine Sun
Department of Pathology, New York University Grossman School of Medicine, New York, NY, USA
1 shared publication- Ke Hu
Department of Pathology, New York University Grossman School of Medicine, New York, NY, USA
1 shared publication Li Zhong
Department of Pathology, New York University Grossman School of Medicine, New York, NY, USA
1 shared publication
Latest Publications
- 20 June 2025
- Published by American Association for the Advancement of Science (AAAS) in Science Immunology
- Vol. 10 (108) , eadq8860
CLNS1A regulates genome stability and cell cycle progression to control CD4 T cell function and autoimmunity
Pathogenic CD4 T cells drive autoimmunity in diseases such as multiple sclerosis (MS) and inflammatory bowel disease (IBD). Through a forward genetic screen, we identified chloride nucleotide-sensitive channel 1A (CLNS1A) as a key regulator of inflammation in the experimental autoimmune encephalomyelitis (EAE) model of MS. CLNS1A is expressed in several subsets of CD4 T cells, including pathogenic T helper 17 (pT H 17) cells. Deletion of Clns1a in T cells resulted in DNA damage, cell cycle arrest, impaired T cell proliferation, and effector function, thereby protecting mice from both EAE and IBD. We found that CLNS1A interacts with protein arginine methyl transferase 5 (PRMT5). Moreover, CLNS1A regulates symmetric histone dimethylation and the expression of genes involved in DNA repair, replication, and cell cycle progression. Thus, CLNS1A plays an important role in CD4 T cells by promoting genome stability and cell cycle progression.
- 20 June 2025
- Published by American Association for the Advancement of Science (AAAS) in Science Immunology
- Vol. 10 (108) , eadq8860
CLNS1A regulates genome stability and cell cycle progression to control CD4 T cell function and autoimmunity
Pathogenic CD4 T cells drive autoimmunity in diseases such as multiple sclerosis (MS) and inflammatory bowel disease (IBD). Through a forward genetic screen, we identified chloride nucleotide-sensitive channel 1A (CLNS1A) as a key regulator of inflammation in the experimental autoimmune encephalomyelitis (EAE) model of MS. CLNS1A is expressed in several subsets of CD4 T cells, including pathogenic T helper 17 (pT H 17) cells. Deletion of Clns1a in T cells resulted in DNA damage, cell cycle arrest, impaired T cell proliferation, and effector function, thereby protecting mice from both EAE and IBD. We found that CLNS1A interacts with protein arginine methyl transferase 5 (PRMT5). Moreover, CLNS1A regulates symmetric histone dimethylation and the expression of genes involved in DNA repair, replication, and cell cycle progression. Thus, CLNS1A plays an important role in CD4 T cells by promoting genome stability and cell cycle progression.