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. 2022 Mar 18;12:4706. doi: 10.1038/s41598-022-08735-7

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© The Author(s) 2022

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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The mechanism of the CVX interaction with the CTLR proposed (Dectin) in the present study. The interaction of CVX with CTLR (1) induces ROS production (2) and NF-κB activation (3). ROS induce the activation of the NLRP3 inflammasome complex (4); stimulating the production (5) and release of the pro-inflammatory cytokine IL-1β (6). The IL-1β production by the interaction of CVX and CTLR, induces the transcription of IL-10 (7); and consequently, its release (8). The interaction of IL-10 with its specific receptor (9), induces JAK-1 phosphorylation (10), initiating signaling via STAT3 (11,12), performing an anti-inflammatory activity, inhibiting transcription (13), production (14) and IL-2 release (15).