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. 2021 Jun 1;11:11456. doi: 10.1038/s41598-021-90872-6

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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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Summary illustration showing the effects of Il6 absence on the testis. The GnRH produced by the hypothalamus stimulates LH secretion by the pituitary, which triggers the testosterone production by Leydig cells in the testicles. In IL6KO mice, we observed an increased testicular SOCS3 expression. We suggest that the increase of SOCS3 leads to an increased production of testosterone, which is converted by the 5⍺-reductase enzyme into its bioactive metabolite (DHT). Enhanced testicular androgens increase spermatogenesis, which is noted by the increased daily sperm production (DSP), leading to the increased number of spermatids and the thicker layer of the seminiferous epithelium. GnRH—gonadotropin-releasing hormone; LH—luteinizing hormone; DHT—dihydrotestosterone; DSP—daily sperm production; SOCS3—suppressor of cytokine signaling 3. Blue dashed arrow indicates a suggestion.