Relationship Between Cartilage Oligomeric Matrix Protein Level and Helper T Cell 17/regulatory T Cell Balance in Patients With Rheumatoid Arthritis
Abstract Objective To explore the correlation among the level of cartilage oligomeric matrix protein(COMP) as well as the balancing relationship of helper T cell 17(Th17) /regulatory T cells(Treg) of serum in patients with Rheumatoid Arthritis (RA). Methods 40 patients with RA in the Second Hospital of Shanxi Medical University from May 2019 to May 2020 were selected as RA group, while 40 healthy subjects were collected as a control group. After collecting their serum, the figure of Th17, as well as Treg cells, were encountered by flow cytometry(FC), and the proportion of Th17/Treg was counted. Cytometric was also used to detect serum interleukin(IL)-17, IL-10 and IL-6 concentration. Enzyme-linked immunosorbent (ELISA)was also applied to track down the concentrations of COMP as well as tumor necrosis factor-α(TNF-α). All indicators above were considered among groups, and the interrelationship between COMP and the expression of various cells as well as related cytokines was analyzed. Results The concentration of COMP, Th17 and Th17/Treg in RA group were higher than those in the control group, while Treg was lower than that in the control group, and the variation was statistically weighty(P<0.05). The levels of IL-17, IL-6 and TNF-α in RA group were higher than those in the control group, while the concentration of IL-2 was smaller than that of the control group, the differences were statistically weighty(P<0.01). Interrelationship analysis displayed that COMP was undeniably correlated with Th17, Th17/Treg, IL-17, IL-6 as well as TNF-α levels(r =0.687, 0.478, 0.759, 0.903, 0.813, all P<0.01). There was a negative correlation between the levels of COMP and Treg, IL-2(r =-0.356, -0.455, all P<0.01). Conclusion Compared with healthy people, COMP in peripheral blood of patients with RA is abnormally high, and there is obvious T cell immune abnormality, suggesting that COMP may participate in the development of RA by regulating Th17/Treg balance.