Language

English

Publication Date

11-26-2024

Journal

Proceedings of the National Academy of Sciences of the United States of America

DOI

10.1073/pnas.2407648121

PMID

39560641

PMCID

PMC11621630

PubMedCentral® Posted Date

11-19-2024

PubMedCentral® Full Text Version

Post-print

Abstract

Dry eye disease (DED) is characterized by a dysfunctional tear film in which the corneal epithelium and its abundant nerves are affected by ocular desiccation and inflammation. Although adaptive immunity and specifically CD4+ T cells play a role in DED pathogenesis, the exact contribution of these cells to corneal epithelial and neural damage remains undetermined. To address this, we explored the progression of a surgical DED model in wild-type (WT) and T cell-deficient mice. We observed that adaptive immune-deficient mice developed all aspects of DED comparably to WT mice except for the absence of functional and morphological corneal nerve changes, nerve damage-associated transcriptomic signature in the trigeminal ganglia, and sustained tear cytokine levels. Adoptive transfer of CD4+ T cells from WT DED mice to T cell-deficient mice reproduced corneal nerve damage but not epitheliopathy. Conversely, T cell-deficient mice reconstituted solely with naïve CD4+ T cells developed corneal nerve impairment and epitheliopathy upon DED induction, thus replicating the WT DED phenotype. Collectively, our data show that while corneal neuropathy is driven by CD4+ T cells in DED, corneal epithelial damage develops independently of the adaptive immune response. These findings have implications for T cell-targeting therapies currently in use for DED.

Keywords

Animals, Dry Eye Syndromes, CD4-Positive T-Lymphocytes, Mice, Disease Models, Animal, Epithelium, Corneal, Cornea, Tears, Mice, Inbred C57BL, Adoptive Transfer, Cytokines, Female, CD4 T cells. autoimmunity. cornea. neuropathy. ocular surface

Published Open-Access

yes

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