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HISTORY
JOHNE'S INFORMATION CENTER - University of Wisconsin Ñ School of Veterinary Medicine



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Thursday, February 15, 2018
MAP DNA detected in 34% of RA samples compared to 8% healthy controls.

Researchers at the University of Central Florida College of Medicine, Orlando, FL hypothesized that Single Nucleotide Polymorphisms (SNPs) in the negative regulators Protein Tyrosine Phosphatase Non-receptor type 2 and 22 (PTPN2/22) lead to a dysregulated immune response, susceptibility to environmental triggers, and continued apoptosis as seen in chronic inflammation in rheumatoid arthritis (RA) and Crohn’s disease (CD).

MAP DNA was detected in 34% of 70 RA patient samples compared to 8% of 48 healthy controls, (p-values ≤ 0.05, OR = 5.74). Combined occurrence of PTPN2:rs478582 and PTPN22:rs2476601 in association with the presence of MAP has significantly increased T-cell response and elevated IFN-γ expression in RA patient samples. The data suggest that genetic polymorphisms may play vital role in T-cell regulation, susceptibility to mycobacteria and ultimately response to treatment. This is the first study to report the detection of MAP DNA in the blood of RA patients; further studies are needed using larger number of samples.

RA is an idiopathic autoimmune disease with suspected genetic predisposition and environmental triggers association. Due to intense inflammation, hyperplasia of the joints occurs along with cartilage and bone destruction, which leads to extreme pain and deformity of the extremities. RA is a common chronic disease that affects about 1% of the world population. The prevalence of RA in the US is estimated at approximately 1.29 million people or 0.6% of the population.

Link to the full article in Frontiers in Cellular and Infection Microbiology