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. 2021 Jan 20;12(1):102. doi: 10.1038/s41419-021-03393-5

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — A, B Serum levels of KIAA1199 (A) and LMW-HA (MW < 100 kDa) (B) in normal subjects (n = 18), inactive RA (n = 27), and active RA (n = 33) patients were determined by ELISA. C Correlation between serum KIAA1199 and LMW-HA was obtained by the Pearson’s coefficient analysis (r = 0.4309, p < 0.0001, n = 78). D, E Synovial levels of KIAA1199 (D) and LMW-HA (E) in normal subjects (n = 9), inactive RA (n = 18), and active RA (n = 22) patients. F Linear correlation between KIAA1199 and LMW-HA in the synovial fluid (r = 0.6532, p < 0.0001, n = 49). G–I TNF-α (G), IL-1β (H), and IL-6 (I) levels in the synovial fluid of normal subjects (n = 9), inactive (n = 18), and active (n = 22) RA patients. J, K Correlation analysis of synovial TNF-ɑ (J), IL-1β (K), IL-6 (L), and KIAA1199, respectively (n = 49). All of the reactions were conducted in triplicate. Data were presented with mean ± SD.