**Margherita Sisto \*, Domenico Ribatti and Sabrina Lisi**

Department of Basic Medical Sciences, Neurosciences and Sensory Organs (SMBNOS), Section of Human Anatomy and Histology, University of Bari "Aldo Moro", 70124 Bari, Italy; domenico.ribatti@uniba.it (D.R.); sabrina.lisi@uniba.it (S.L.)

**\*** Correspondence: margherita.sisto@uniba.it; Tel.: +39-080-547-8315; Fax: +39-080-547-8327

Received: 3 July 2020; Accepted: 28 August 2020; Published: 31 August 2020

**Abstract:** Sjögren's syndrome (SS) is a systemic autoimmune inflammatory disease with a poorly defined aetiology, which targets exocrine glands (particularly salivary and lachrymal glands), affecting the secretory function. Patients suffering from SS exhibit persistent xerostomia and keratoconjunctivitis sicca. It is now widely acknowledged that a chronic grade of inflammation plays a central role in the initiation, progression, and development of SS. Consistent with its key role in organizing inflammatory responses, numerous recent studies have shown involvement of the transcription factor nuclear factor κ (kappa)-light-chain-enhancer of activated B cells (NF-κB) in the development of this disease. Therefore, chronic inflammation is considered as a critical factor in the disease aetiology, offering hope for the development of new drugs for treatment. The purpose of this review is to describe the current knowledge about the NF-κB-mediated molecular events implicated in the pathogenesis of SS.

**Keywords:** Sjögren's syndrome; NF-κB; inflammation
