Authors
Kaitlin K Scholand, Paola A Guevara Montoya, Emre Aksan, Yangluowa Qu, Sean Paiboonfungfuang, Laura Schaefer, Elizaveta A Demianova, Elaine Vo, Sudhir Verma, Elle Joy J San Juan, Zhiyuan Yu, Tarsis F Gesteira, Vivien J Coulson-Thomas, Cintia S de Paiva
Published in
Mucosal immunology. Pages 100419. Oct 08, 2026. Epub Oct 08, 2026.
Abstract
Sjögren disease (SjD) is an autoimmune disease driven by autoimmune CD4+T cells that leads to an immune-mediated loss of lacrimal glands (LG). Meibomian glands are lipid-producing glands in the eyelids that help prevent tear evaporation. While the role of T cells in LG-mediated destruction is well established, it is unknown whether pathogenic T cells can cause MG dysfunction (MGD). Herein, we investigated whether autoimmune CD4+T cells induce MGD and characterized the pathophysiologic mechanisms using an adoptive transfer model. T cells were isolated from CD25KO (KOCD4) or wild-type (WTCD4) mice and transferred into Rag1KO mice. In comparison, KO cells were co-adoptively transferred with WT regulatory T cells (KOCD4 + WTTregs). Our results demonstrate that CD25KO CD4+T recipients had MG dropout, CD4+IFN-γ+ infiltration, increased MHC II presentation within the periglandular area, MG fibrosis, decreased lipid production, and upregulation of pathways related to inflammation, including Type II interferon signaling. Rag1KO, WTCD4, and KOCD4 + WTTregs recipients exhibited minimal inflammation in the periglandular MG area. These results indicate that autoimmune CD4+T cells are sufficient to cause MGD, and healthy young regulatory T cells can prevent T-cell-mediated damage. Our findings provide mechanistic insights into the pathogenesis of autoimmune SjD and could impact how patients are managed in the clinic.
PMID:
42849738
Bibliographic data and abstract were imported from PubMed on 09 Oct 2026.
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