REVIEW

Use of localised gene transfer to develop new treatment strategies for the salivary component of Sjögren’s syndrome

M R Kok^1,2, B J Baum¹, P P Tak², S R Pillemer¹

¹ Gene Therapy and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA
² Division of Clinical Immunology and Rheumatology, Academic Medical Centre/University of Amsterdam, Amsterdam, The Netherlands

Correspondence to:
Correspondence to:
Dr M R Kok, Meibergdreef 9, Room F4-218, 1105 AZ, Amsterdam, The Netherlands;
m.r.kok{at}amc.uva.nl

Effective treatment for Sjögren’s syndrome (SS) might be developed locally by introducing genes encoding cytokines, which are potentially anti-inflammatory, or by introducing a cDNA encoding a soluble form of a key cytokine receptor, which can act as an antagonist and decrease the availability of certain cytokines, such as soluble tumour necrosis factor receptors. Currently, the preferred choice of viral vector for immunomodulatory gene transfer is recombinant adeno-associated virus. The use of gene transfer to help determine the pathophysiology and to alter the course of the SS-like disease in the NOD mouse model can ultimately lead to the development of new treatments for managing the salivary component in patients with SS.

Keywords: salivary gland; autoimmune disease; gene transfer; adeno-associated virus; immunotreatment

Abbreviations: AAV, adeno-associated virus; BLyS, B lymphocyte stimulation; ICAM, intercellular adhesion molecule; IFN, interferon ; IL, interleukin; LFA, leucocyte function associated antigen; MHC, major histocompatibility complex; NOD, non-obese diabetic; RA, rheumatoid arthritis; rAAV, recombinant adeno-associated virus; RT-PCR, reverse transcription-polymerase chain reaction; SCID, severe combined immunodeficiency; SS, Sjögren’s syndrome; TNF, tumour necrosis factor ; VCAM, vascular cell adhesion molecule

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