**1. Introduction**

The nuclear factor κ (kappa)-light-chain-enhancer of activated B cells (NF-κB) is a pleiotropic regulator of many cellular signalling pathways activated in response to a wide variety of stimuli linked to inflammation. Once activated, this B cell enhancer plays an important role in the pathogenesis of several inflammatory autoimmune diseases, including Sjögren's syndrome (SS) [1]. SS presents lymphocytic infiltration of the salivary glands (SGs) and lachrymal glands as the characteristic hallmark resulting in chronic inflammation. A dry mouth and dry eyes, resulting in keratoconjunctivitis sicca and xerostomia, are common complaints in SS [2]. NF-κB is a family of DNA-binding proteins that regulates many cellular processes, notably the immune response and inflammation, influencing the transcription of a broad array of pro-inflammatory cytokines [3]. NF-κB is ubiquitously expressed in SGs, and the constitutive NF-κB activation observed in primary SS (pSS) is associated with NF-κB release and nuclear translocation of NF-κB, to focal infiltrated lymphocytes and the acinar epithelium of patients with pSS, to regulate the pro-inflammatory gene transcriptions [4]. However, the role of NF-κB in pSS remains to be clarified in detail. This article provides an update on the current state of knowledge about the relationship between NF-κB-molecular pathway activation in SGs and the chronic inflammation characterizing pSS, with the aim of providing a strong basis for a better understanding of the signal transduction pathways mediating the induction of NF-κB in pSS SGs, in order to allow this disease to be manipulated, to gain therapeutic benefit.
