Transcriptomic Changes in the Lacrimal Glands of a Sjogren's Disease Animal Model Highlight Key Molecular Mediators and Altered Biological Functions Underpinning Glandular Inflammation and Hypofunction

Insufficient or low-grade tear secretion onto the ocular surface affects the normal physiology of the cornea and conjunctiva and can result in ocular surface damage. Herein, we evaluated the transcriptomic profiles of diseased versus healthy LGs to investigate the underlying molecular mechanisms underscoring LG autoimmune inflammation and secretory hypofunction.

The number of differentially expressed genes between NOR (diseased animal model/strain) and BALB/c (control strain) mice increased in correlation with the development and progression of dacryoadenitis. The most significantly upregulated pathways were primarily related to immune responses, emphasizing the activation of cellular and cytokine-mediated inflammatory responses. Several cytokines, transcription factors, and toll-like receptors were significantly predicted to drive most of the differential gene expression observed across our datasets.