Newly identified association between single nucleotide polymorphisms and intestinal bacteria in rheumatoid arthritis patients may provide new approaches for treatment
Rheumatoid arthritis (RA) is a chronic inflammatory disease that has been linked to infectious agents such as the bacteria, Mycobacterium avium subspecies paratuberculosis (MAP). While the exact cause of RA is unknown, genetic predisposition is also thought to play a major role. Polymorphisms in several genes that regulate the immune system have been associated with RA development.
UCF researchers are studying the molecular mechanism of inflammation in RA. They have identified several single nucleotide polymorphisms (SNPs) in the immune regulatory genes Protein Tyrosine Phosphatase Non-Receptor Type 2 and 22 (PTPN2/22) that along with MAP infection may promote inflammation in RA patients. The identified SNPs in PTPN2/22 were found in RA patients and associated with a dysregulated immune system and increased susceptibility to MAP infection. Combination therapies targeting both inflammation and bacterial infection may provide more effective treatments for RA.
Personalized treatment for RA by genetic testing for SNPs and antibiotic treatment for MAP infection
New markers and targets for diagnosis and treatment of RA
Polymorphisms in Protein Tyrosine Phosphatase Non-receptor Type 2 and 22 (PTPN2/22) Are Linked to Hyper-Proliferative T-Cells and Susceptibility to Mycobacteria in Rheumatoid Arthritis, Frontiers in Cellular and Infection Microbiology, January 25, 2018, Volume 8, Article 11