AB0335 THE CORRELATION OF CORRELATION OF TH17 AND TREG CELL LEVELS OF IN CORONARY HEART DISEASE PATIENTS WITH RHEUMATOID ARTHRITIS
Authors: Yue Teng Ma, Sheng Xiao Zhang
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Rheumatoid arthritis (RA) is a prevalent chronic autoimmune inflammatory disease. Also acute coronary syndrome (ACS) is a prevalent chronic inflammatory disease. Now more and more studies have also shown that coronary heart disease is also associated with immune inflammationWe will discuss Th17 and Treg cell levels in patients with rheumatoid arthritis combined with coronary heart disease and simple rheumatoid joints as well as normal people. Its pathogenesis is closely associated with a failure of endogenous immune tolerance that caused by the imbalance of CD4/CD8.New T subgroup Th17 Treg,T lymphocytes play an important role in the occurrence and development of RA and ACS,Moreover, T lymphocytes are one of the first cells to be recruited into atherosclerotic plaques<sup>1</sup>, and most adhesion molecules and chemokines that promote the migration of monocytes to the intima are also related to T cell recruitment.T lymphocytes mainly divided into two major subsets of CD4/CD8, including CD4 <sup>+</sup>T helper cells, which are classified into Th1Th2 and newly discovered Th17 cells and regulatory T cells subgroup, have the effect of the immune response to promote the immune, and CD8 <sup>+</sup>play the role of killer cells and suppress the immune response,Similar to CD8, (Treg) lymphocytes can reduce the body's anti-tumor ability by inhibiting cell contact and the production of inhibitory factors and effector T cells <h3>Objectives</h3> Through clinical studies, we want to explore whether the proportion of Th17/Treg in peripheral blood of RAwithACSpatients is reduced to indicate whether the immune balance is broken, thus providing further data for clinical studies <h3>Methods</h3> In April 2017 to September 2018 in our hospital Patients with RAand ACS diagnosed by Coronary angiography in our hospital of 20 cases male:9 female:12 into the research object, the diagnosis of ACS combined with clinical data of 20 patients as Observation group, These patients have been diagnosed with rheumatoid arthritis. Another 20 rheumatoid arthritis patientsmale: 11 female:9were collected from the rheumatology department of our hospital, and 20 normal healthy peoplemale:10female:10 were collected from the physical examination center of our hospital,as control group Chart-1 Chart-2 <h3>Results</h3> Compared with the control group, the proportion of Th17 cells and Treg cells in peripheral blood of RA with ACS and RA groups increased and decreased respectively (P &lt; 0.05).Compared with the RA group, the proportion of Th17 cells in the peripheral blood of RA with ACS group increased, while the proportion of Treg cells decreased (P &lt; 0.05).The proportion of Th17 cells in RA with ACS group was higher than that in RA group and control group (P &lt; 0.05).Th17/Treg ratio in control group, RA group, ACS and RA groups were, respectively Compared with the control group, Th17/Treg increased in the RA with ACS and RA groups, and the RA with ACS group was higher than the RA group, with statistically significant differences (P &lt; 0.05),but the ratio between the RA group and the control group was not significant <h3>Conclusion</h3> Through this rare clinical study, it was found that the levels of Treg cells and Th17 cells in patients with rheumatoid arthritis combined with coronary heart disease were to some extent higher than those in patients with rheumatoid arthritis alone and normal healthy people.We can speculate whether it is possible to find a target for Treg cell Th17 cell levels in patients with RA with ACS expanding the sample study again, so as to intervene as early as possible and regulate the immune balance to avoid the progression of coronary heart disease and adverse cardiovascular events <h3>References</h3> [1] Libby, P.; Ridker, P. M.; Hansson, G. K.; Leducq Transatlantic Network on, A., Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol 2009, 54 (23), 2129-38. <h3>Acknowledgement</h3> None <h3>Disclosure of Interests</h3> None declared