Abstract

<h3>Background</h3> Relapsing polychondritis (RP) is an rare inflammatory disease of unknown causes, characterized by recurrent inflammation in cartilaginous tissues of the whole body<sup>[1]</sup>. The histologic features of the chondritis include loss of basophilic staining of the cartilage matrix, perichondrial inflammation, cartilage destruction with replacement by fibrous tissue, and perivascular cellular infiltration with plasma cells and lymphocytes. Additional clinical features of the disease include ocular inflammation, vasculitis, audiovestibular dysfunction, myocarditis, cardiac valvular insufficiency, and nonerosive inflammatory arthritis. Many studies have shown that the imbalance of helper T cell 17(Th17) and regulatory T cell(Treg) is involved in the pathogenesis of autoimmune diseases such as SLE and RA. But little is known about the roles of peripheral immune cell subsets peripheral in RP patients. Up to now, just few studies focus on this issue. <h3>Objectives</h3> We aimed to analyse the distribution and phenotype of CD4+T cell subsets in the peripheral blood of patients with RP. <h3>Methods</h3> The proportion and absolute counts of circulating immune cells were assessed in 14 patients diagnosed as RP and 14 healthy controls. CD4+T cell subsets were also analysed in 9 untreated RP patients and 9 healthy volunteers by flow cytometry. All statistical analyses were performed with SPSS v. 22.0. Continuous variables were reported as median. For all study variables, comparison among controls and RP subjects was based on the non-parametric Wilcoxon Mann-Whitney exact test. For all analyses, we used two-sided tests, with p-values &lt;0.05 denoting statistical significance. <h3>Results</h3> Proportion and absolute counts of Treg cells were significantly reduced in RP patients in comparison with controls (proportion, 3.61% vs. 5.24%, p&lt;0.001; absolute counts, 27.36/μl vs. 46.56/μl,p&lt;0.001). But there were no significant difference between the percentage and number of Th17, Th1 or Th2 cells in patients with RP and healthy controls. Thus, the ratio of Th17/Treg increased in RP patients (0.25 vs. 0.14, p&lt;0.001), as did the ratio of Th2/Treg (0.28 vs. 0.22, p&lt;0.001) and Th1/Treg(2.75 vs. 1.92, p=0.019)(Figue 1). Similarly, the proportion and absolute counts of Treg cells in untreated RP patients were significantly lower than that in healthy controls (proportion, 3.78% vs. 5.66%, p=0.008; absolute counts, 32.24/μl vs. 50.76/μl, p&lt;0.001).And the ratio of Th17/Treg slso increased in untreated RP patients (0.25 vs. 0.15, p=0.003), as did the ratio of Th1/Treg (2.35 vs. 1.88, p=0.014)(Figue 2). <h3>Conclusion</h3> Our data suggested that the immune-inflammation in RP patients may be related to the depletion of Treg cells and the imbalance of Th17 or Th1 or Th2 and Treg cells.Reduction of peripheral Treg cells may exacerbate the disease progression by not being inhibited Th cells. <h3>Reference</h3> [1] Kingdon J, Roscamp J, Sangle S, et al. Relapsing polychondritis: a clinical review for rheumatologists[J]. Rheumatology, 2017, 57(9): 1525-1532. <h3>Acknowledgement</h3> Rheumatology and laboratory staff in the Second Hospital of Shanxi Medical University <h3>Disclosure of Interests</h3> None declared

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