Transforming growth factor β1 gene polymorphism in rheumatoid arthritis
- 1Second Department of Internal Medicine, Nagoya City University, Medical School, Nagoya, Japan
- 2Second Department of Pathology, Nagoya City University, Medical School
- Correspondence to:
T Niimi, Second Department of Internal Medicine, Nagoya City University, Medical School, Kawasumi 1, Mizuho-ku, Nagoya-city, Aichi 467–8601, Japan
- Accepted 25 February 2002
Objective: Rheumatoid arthritis (RA) is a chronic inflammatory disease and synovial cells, antigen presenting cells, lymphocytes, and their cytokines might be associated with the disease. Transforming growth factor β1 (TGFβ1) has been reported to have important roles in unresolved inflammation, immune suppression, fibrosing processes, and angiogenesis. TGFβ1 is highly expressed in joints in RA and is considered to be a regulator of anti-inflammation in RA. Polymorphisms of TGFβ1 have been reported to be associated with the production of TGFβ1 protein, and to increase the risk of acquiring several diseases. It was speculated that these polymorphisms might also be involved in RA, and therefore the TGFβ1 codon 10 T869C polymorphism in a series of patients and controls was investigated.
Method: A total of 155 patients with RA and 110 healthy subjects were studied. DNA was extracted from peripheral leucocytes and TGFβ1 codon 10 T869C polymorphism was determined by polymerase chain reaction restriction fragment polymorphism.
Results: A significantly higher proportion of patients with RA with the T allele (CT type or TT type) was found compared with the CC type (p=0.039).
Conclusion: The T allele, previously reported to be linked with production of TGFβ1, may be associated with an increased risk of RA.
- PCR-RFLP, polymerase chain reaction restriction fragment length polymorphism
- TGFβ, transforming growth factor β