Sjögren’s Syndrome: Exocrine Gland-Targeted Autoimmunity
Sjögren’s syndrome affects approximately 3 million Americans, causing immune-mediated destruction of salivary and lacrimal glands resulting in dry mouth, dry eyes, and systemic complications. Like other autoimmune conditions, environmental triggers including chemical exposures may initiate or accelerate the autoimmune process in predisposed individuals.
PFAS and Glandular Epithelial Immune Activation
PFAS accumulate in glandular tissue and alter epithelial cell immune signaling. PFAS-induced upregulation of Ro/SSA and La/SSB antigens—the target autoantigens in Sjögren’s syndrome—may lower the threshold for autoimmune recognition of glandular tissue in immunogenetically susceptible HLA-DR3-positive individuals.
Lymphocytic Infiltration and PFAS
Lymphocytic infiltration of exocrine glands is the histological hallmark of Sjögren’s syndrome. PFAS exposure promotes interferon-alpha production and B-cell hyperactivation—mechanisms central to Sjögren’s pathogenesis. Elevated interferon signatures are documented in both PFAS-exposed populations and Sjögren’s patients.
Clinical Recognition
Rheumatologists evaluating Sjögren’s syndrome patients in PFAS-affected areas should document water source history. Sicca symptoms (dry eye/mouth) in patients with detectable PFAS exposures and appropriate autoantibody profiles deserve comprehensive Sjögren’s workup, with exposure reduction as a potential modifier of disease activity.