The T cell in Sjogren's syndrome: force majeure, not spectateur

J Autoimmun. 2012 Sep;39(3):229-33. doi: 10.1016/j.jaut.2012.05.019. Epub 2012 Jun 17.


Sjogren's syndrome (SS) is characterized by infiltration of exocrine glands with T and B lymphocytes, leading to glandular dysfunction and frequently accompanied by hypergammaglobulinemia and autoantibodies. The role of T cells, which predominate in the lesions, has attracted much interest. CD4 T cells seem to be responding to autoantigens on apoptotic cells, such as the Ro and La antigens, or to the cytoskeletal antigen α-fodrin. Physical injury to ocular surfaces may also lead to T cell mediated responses to self antigens and perpetuate disease. Within the salivary glands, T cell responsiveness is further promoted by the special capacity of salivary epithelial tissue to provide costimulation and enhanced antigen presentation. Cytokines are key mediators of the T cell contribution to pathology, with roles attributed both to Th1 and Th2 cells. Recently, striking data implicate Th17 cells in the stimulation of B cells, and a role for the related cytokine IL-21 produced by follicular T helper cells is now appreciated. Dysfunction of T regulatory cells has been shown to have a role in the exuberant production of cytokines by Th17 cells. Beyond their role in provoking B cell hyperactivity and immunoglobulin secretion, T cells are directly involved in destruction of glands through Fas and perforin-mediated cytotoxicity. Animal models of SS have confirmed the role of T cell derived cytokines in disease and support a role for effector-memory cells in pathogenesis. Further elucidation of the role of T cells will open avenues for better treatment of SS, whose current management is still mainly supportive.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / immunology
  • Autoantibodies / biosynthesis
  • Autoantibodies / immunology*
  • Autoantigens / immunology
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism
  • B-Lymphocytes / pathology
  • Cell Communication / immunology
  • Humans
  • Interleukins / biosynthesis
  • Interleukins / immunology
  • Lymphocyte Activation
  • Mice
  • Perforin / genetics
  • Perforin / immunology
  • Salivary Glands / immunology*
  • Salivary Glands / metabolism
  • Salivary Glands / pathology
  • Sjogren's Syndrome / immunology*
  • Sjogren's Syndrome / metabolism
  • Sjogren's Syndrome / pathology
  • T-Lymphocyte Subsets / immunology*
  • T-Lymphocyte Subsets / metabolism
  • T-Lymphocyte Subsets / pathology
  • fas Receptor / genetics
  • fas Receptor / immunology


  • Autoantibodies
  • Autoantigens
  • FAS protein, human
  • Interleukins
  • fas Receptor
  • Perforin
  • interleukin-21