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Experience with experimental biological treatment and local gene therapy in Sjögren’s syndrome: implications for exocrine pathogenesis and treatment
  1. B M Lodde1,2,
  2. B J Baum1,
  3. P P Tak2,
  4. G Illei1
  1. 1Gene Therapy and Therapeutics Branch/NIDCR, National Institutes of Health, DHHS, Bethesda, Maryland, USA
  2. 2Clinical Immunology and Rheumatology, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands
  1. Correspondence to:
    G Illei
    Gene Therapy and Therapeutics Branch/NIDCR, National Institutes of Health, 10 Center Drive, Building 10, Room 1N114, Bethesda, MD 20892-1190, USA; gillei{at}mail.nih.gov

Abstract

Sjögren’s syndrome is an autoimmune exocrinopathy, mainly affecting the lacrimal and salivary glands, and resulting in ocular and oral dryness (keratoconjunctivitis sicca and xerostomia). The aetiology and pathogenesis are largely unknown, and only palliative treatment is currently available. Data obtained from experimental animal and human studies using biological agents or gene therapeutics can offer insight into the disease process of Sjögren’s syndrome. This article reviews the current literature on these approaches and assesses the lessons learnt about the pathogenesis of Sjögren’s syndrome.

  • AAV, adeno-associated virus
  • BAFF, B cell-activating factor
  • FasL, Fas ligand
  • IFN, interferon
  • MALT, mucosa-associated lymphoid tissue
  • NFκB, nuclear factor κB
  • NOD, non-obese diabetic
  • rAAV2, recombinant serotype 2 AAV vector
  • RANTES, regulated on activation, normal T cell expressed and secreted
  • SMG, submandibular gland
  • TNF, tumour necrosis factor
  • TNFRp55-Ig, human 55-kDa TNF receptor extracellular domain linked to a mouse IgG heavy chain
  • VIP, vasoactive intestinal peptide

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Footnotes

  • Published Online First 31 July 2006

  • Funding: This research was supported by the Intramural Research Program of the NIDCR/NIH.

  • Competing interests: None.

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