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Pathogenesis of primary Sjögren's syndrome beyond B lymphocytes


1, 2, 3, 4, 5, 6, 7, 8

 

  1. Division of Rheumatology, Department of Precision Medicine, University of Campania Luigi Vanvitelli, Naples, Italy.
  2. Division of Rheumatology, Department of Precision Medicine, University of Campania Luigi Vanvitelli, Naples, Italy.
  3. Division of Rheumatology, Department of Precision Medicine, University of Campania Luigi Vanvitelli, Naples, Italy.
  4. Department of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, China.
  5. Department of Rheumatology, Peking Union Medical College Hospital, Beijing, China.
  6. Department of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, China.
  7. Dipartimento Biomedico di Medicina Interna e Specialistica, Section of Rheumatology, University of Palermo, Italy.
  8. Division of Rheumatology, Department of Precision Medicine, University of Campania Luigi Vanvitelli, Naples, Italy. francesco.ciccia@unicampania.it

CER13731
2020 Vol.38, N°4 ,Suppl.126
PI 0315, PF 0323
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PMID: 33095148 [PubMed]

Received: 25/06/2020
Accepted : 04/09/2020
In Press: 23/10/2020
Published: 23/10/2020

Abstract

Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disorder affecting exocrine glands of the body, prevalently lacrimal and salivary glands. The pSS pathogenesis has been thought to be B-cell-centric and several clinical trials have been carried out in order to clarify the therapeutic role of B-cell depletion in patients with pSS. Unfortunately, however, B-cell depletion with rituximab has failed in demonstrating any significant results in pSS patients. Besides the contribution of B cells in the pathogenesis of pSS, effector Tfh, Th17 and Th22 cells, follicular dendritic cells (DCs), innate cells (ICs) and several cytokines, chemokines and miRNA have been proved to participate to the development of this systemic disease. Understanding these molecular processes may help guide research into resistant diseases and highly targeted therapeutic strategies. This review aims to discuss important pathogenetic mechanisms involved in the initiation and perpetuation of pSS behind the established role of B cells.

Rheumatology Article