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Claudin-11 regulates immunological barrier formation and spermatogonial proliferation through stem cell factor
Taichi Sugawara1, Kayoko Sonoda2, Nattapran Chompusri2
1Department of Histology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. tsugawara@kumamoto-u.ac.jp.
Communications Biology
|January 30, 2025
Summary
Claudin-11 (CLDN11) is crucial for Sertoli cell tight junctions (SCTJs), maintaining male fertility. Loss of CLDN11 disrupts spermatogenesis by impairing Sertoli cell polarization and stem cell factor localization.
Area of Science:
- Reproductive Biology
- Immunology
- Cell Biology
Background:
- Sertoli cell tight junctions (SCTJs) are hypothesized to create an immune barrier protecting developing sperm cells.
- Direct evidence for the immunological function of SCTJs is lacking.
Purpose of the Study:
- To investigate the role of claudin-11 (CLDN11) in Sertoli cell tight junctions and male reproductive immunology.
- To determine if CLDN11 deficiency impacts spermatogenesis and immune responses to sperm antigens.
Main Methods:
- Analysis of male mice lacking CLDN11, including crosses with recombination activating gene 2 (Rag2) knockout mice.
- Detection of autoantibodies against spermatogenic cell antigens.
- Assessment of Sertoli cell polarization, stem cell factor (SCF) localization, and spermatogonial proliferation.
Main Results:
- Mice lacking CLDN11 developed autoantibodies against spermatocyte and spermatid antigens.
- Impaired spermatogenesis in CLDN11-deficient mice was independent of mature T and B lymphocytes.
- CLDN11 deficiency disrupted Sertoli cell polarization, SCF localization, and spermatogonial proliferation.
Conclusions:
- CLDN11 is essential for Sertoli cell tight junction integrity and Sertoli cell polarization.
- CLDN11-mediated Sertoli cell polarization establishes a microenvironment for stem cell factor signaling, crucial for spermatogonial proliferation and male fertility.
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