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Pathogenesis of Sjögren's Syndrome: Characteristics of Different Mouse Models for Autoimmune Exocrinopathy

2002; Elsevier BV; Volume: 103; Issue: 2 Linguagem: Inglês

10.1006/clim.2002.5189

1521-7035

Saskia C A van Blokland, Marjan A. Versnel,

Galectins and Cancer Biology

Data across various dry eye disease models consistently demonstrate that aberrant ocular surface inflammation is a characteristic disease phenotype as well as a key pathogenic component actively mediating the disease initiation, perpetuation, and sustention, primarily anchored on the principal effectors of autoreactive CD4+ T-cells. Initial T-cell activation occurs in the local lymphoid compartment, and is closely orchestrated by rapid innate response of ocular surface resident cells to various “danger signals” that are associated with sex hormones, aging, nerve-derived factors, or microbiome. Activated T cells are resistant to the dysfunctional immunoregulatory mechanisms, and subsequently home to the ocular surface facilitated by chemokines and adhesion molecules, exerting pathogenic roles via direct self-tissue damage and further amplification of inflammatory cascade. Finally, long-term T-cell memory is formed and maintains the disease chronicity. Collectively, this preclinical knowledge suggests that restoration of ocular immune homeostasis can be the key to effectively treat or cure the disease.