3.2.1. Upregulation of Adhesion Molecules

According to recent observations, several SS pathogenic models could explain the role of SGEC in glandular damage. The current SS pathogenic model is the "autoimmune epithelitis". This model considers SGEC as a crucial player in the initial triggering phase of the disease [86]. SGEC from SS patients express significantly higher levels of TLRs mRNA levels, including TLR-1, TLR-2, TLR-3 and TLR-4 as compared to control SGEC [87]. Under physiological conditions, TLRs are activated by the recognition of pathogen-associated molecular patterns (PAMPs) derived from microorganisms and endogenous mediators of inflammation known as danger-associated molecular patterns (DAMPs) [88]. TLR signalling pathway acts as link between innate and adaptive immunity in autoimmune diseases. Indeed, upon activation, TLRs recruit adapter proteins in order to propagate the intracellular signal that results in the transcription of genes involved in inflammation, immune regulation, cell survival and proliferation and subsequent activation of the immune system. TLR signalling in SGEC upregulates several molecules such as MHC class I and class II, costimulatory molecules such as B7.1 (CD80) and B7.2 (CD86) and adhesion molecules 1 (ICAM-1) [89].
