| First Author | Sardar S | Year | 2019 |
| Journal | Arthritis Res Ther | Volume | 21 |
| Issue | 1 | Pages | 16 |
| PubMed ID | 30630509 | Mgi Jnum | J:295093 |
| Mgi Id | MGI:6459635 | Doi | 10.1186/s13075-018-1797-3 |
| Citation | Sardar S, et al. (2019) The oncoprotein TBX3 is controlling severity in experimental arthritis. Arthritis Res Ther 21(1):16 |
| abstractText | BACKGROUND: Development of autoimmune diseases is the result of a complex interplay between hereditary and environmental factors, with multiple genes contributing to the pathogenesis in human disease and in experimental models for disease. The T-box protein 3 is a transcriptional repressor essential during early embryonic development, in the formation of bone and additional organ systems, and in tumorigenesis. METHODS: With the aim to find novel genes important for autoimmune inflammation, we have performed genetic studies of collagen-induced arthritis (CIA), a mouse experimental model for rheumatoid arthritis. RESULTS: We showed that a small genetic fragment on mouse chromosome 5, including Tbx3 and three additional protein-coding genes, is linked to severe arthritis and high titers of anti-collagen antibodies. Gene expression studies have revealed differential expression of Tbx3 in B cells, where low expression was accompanied by a higher B cell response upon B cell receptor stimulation in vitro. Furthermore, we showed that serum TBX3 levels rise concomitantly with increasing severity of CIA. CONCLUSIONS: From these results, we suggest that TBX3 is a novel factor important for the regulation of gene transcription in the immune system and that genetic polymorphisms, resulting in lower expression of Tbx3, are contributing to a more severe form of CIA and high titers of autoantibodies. We also propose TBX3 as a putative diagnostic biomarker for rheumatoid arthritis. |
