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. 2021 Apr 12;11:7937. doi: 10.1038/s41598-021-87199-7

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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CCL11 stimulation induced CCL11 and CCR3 mRNA. (A) RA FLS were stimulated with 200 ng/mL CCL11 for 12, 24 and 48 h. The expression of CCL11 mRNA at 48 h was induced by CCL11 self-stimulation (n = 5 patients). (B) The expression of CCR3 mRNA at 48 h was induced by CCL11 stimulation (n = 5 patients). (C) An antagonist of CCR3 (SB328437) at 100 µM reduced TNF-α-induced CCL11 secretion from RA FLS (n = 3 patients). NS no stimulation. The data are expressed as the mean ± SEM. *p < 0.05 was significant.