Previous reports have shown an increase in IFN-γ, CXCL9 and CXCL10 in the salivary gland epithelial cells of SS patients, as well as constant infiltration of CTLs in inflammatory lesions in salivary glands in the female NOD murine model, which is representative of SS (35) IFN-γ derived from CTLs can alter tight junction integrity and function in parotid epithelial cells, leading to cell death (70, 71) (Figure 1). This evidence concerns the gene CXCL10 and synovial sarcoma.