Use of localised gene transfer to develop new treatment strategies for the salivary component of Sjögren’s syndrome
- 1Gene Therapy and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA
- 2Division of Clinical Immunology and Rheumatology, Academic Medical Centre/University of Amsterdam, Amsterdam, The Netherlands
- Correspondence to:
Dr M R Kok, Meibergdreef 9, Room F4-218, 1105 AZ, Amsterdam, The Netherlands;
m.r.kokamc.uva.nl
- Accepted 1 May 2003
Abstract
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 α 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.
- AAV, adeno-associated virus
- BLyS, B lymphocyte stimulation
- ICAM, intercellular adhesion molecule
- IFNγ, interferon γ
- 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
- TNFα, tumour necrosis factor α
- VCAM, vascular cell adhesion molecule








