Epithelial-immune cell interplay in primary Sjögren syndrome salivary gland pathogenesis.

摘要: In primary Sjogren syndrome (pSS), the function of salivary glands is often considerably reduced. Multiple innate immune pathways are likely dysregulated in gland epithelium pSS, including nuclear factor-κB pathway, inflammasome and interferon signalling. The ductal cells pSS characteristically surrounded by a CD4+ T cell-rich B infiltrate, implying degree communication between epithelial cells. cell infiltrates within ducts can initiate development lymphoepithelial lesions, basal hyperplasia. Vice versa, provides chronic activation signals to glandular fraction. This continuous stimulation might ultimately drive mucosa-associated lymphoid tissue lymphoma. Review discusses changes (including acinar, progenitor cells), proposed interplay these with environmental stimuli system. Current therapeutic options insufficient address both lymphocytic infiltration dysfunction. Successful rescue will probably demand multimodal approach an appreciation complicity pSS.