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<p>Tight junctions (TJs) between adjacent Sertoli cells are believed to form immunological barriers that protect spermatogenic cells expressing autoantigens from autoimmune responses. However, there is no direct evidence that Sertoli cell TJs (SCTJs) do indeed form immunological barriers. Here, we analyzed male mice lacking claudin-11 (<i>Cldn11</i>), which encodes a SCTJ component, and found autoantibodies against antigens of spermatocytes/spermatids in their sera. Defective spermatogenesis in <i>Cldn11</i>-deficient mice was not restored on a recombination activating gene 2 (<i>Rag2</i>) knockout background lacking mature T and B lymphocytes. This suggests that adaptive immune responses to spermatogenic cells are not a cause of defective spermatogenesis in <i>Cldn11</i>-deficient mice. Further analyses showed that <i>Cldn11</i> knockout impaired Sertoli cell polarization, localization of stem cell factor (SCF) (a key molecule for maintaining differentiating spermatogonia) to the basal compartment of seminiferous tubules, and also proliferation of differentiating spermatogonia. We propose that CLDN11 creates a microenvironment for SCF-mediated spermatogonial proliferation at the basal compartment via Sertoli cell polarization.</p>

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Claudin-11 regulates immunological barrier formation and spermatogonial proliferation through stem cell factor

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月30日

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  • Taichi Sugawara,
  • Kayoko Sonoda,
  • Nattapran Chompusri,
  • Kazuhiro Noguchi,
  • Seiji Okada,
  • Mikio Furuse,
  • Tomohiko Wakayama

摘要

Tight junctions (TJs) between adjacent Sertoli cells are believed to form immunological barriers that protect spermatogenic cells expressing autoantigens from autoimmune responses. However, there is no direct evidence that Sertoli cell TJs (SCTJs) do indeed form immunological barriers. Here, we analyzed male mice lacking claudin-11 (Cldn11), which encodes a SCTJ component, and found autoantibodies against antigens of spermatocytes/spermatids in their sera. Defective spermatogenesis in Cldn11-deficient mice was not restored on a recombination activating gene 2 (Rag2) knockout background lacking mature T and B lymphocytes. This suggests that adaptive immune responses to spermatogenic cells are not a cause of defective spermatogenesis in Cldn11-deficient mice. Further analyses showed that Cldn11 knockout impaired Sertoli cell polarization, localization of stem cell factor (SCF) (a key molecule for maintaining differentiating spermatogonia) to the basal compartment of seminiferous tubules, and also proliferation of differentiating spermatogonia. We propose that CLDN11 creates a microenvironment for SCF-mediated spermatogonial proliferation at the basal compartment via Sertoli cell polarization.