2. Academic Validation
  3. Recombinant humanized type I collagen remodels decidual immune microenvironment at maternal-fetal interface by modulating Th17/Treg imbalance

Recombinant humanized type I collagen remodels decidual immune microenvironment at maternal-fetal interface by modulating Th17/Treg imbalance

  • Int J Biol Macromol. 2024 Sep;276(Pt 2):133994. doi: 10.1016/j.ijbiomac.2024.133994.
Li Wang 1,  Hui Zeng 1,  Hu Li 1,  Jingcong Dai 1,  Shuang You 1,  Huanhuan Jiang 2,  Quan Wei 1,  Zhiyong Dong 1,  Shuaibin Liu 1,  Ju Ren 1,  Yun Zhu 3,  Xia Yang 4,  Fan He 5,  Lina Hu 6
Affiliations

Affiliations

  • 1 Department of Obstetrics and Gynaecology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
  • 2 Yangzhou Maternal and Child Care Service Centre, Yangzhou 225000, Jiangsu, China.
  • 3 National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
  • 4 Shanxi Key Laboratory of Functional Proteins, Shanxi Jinbo Bio-Pharmaceutical Co., Ltd., Taiyuan 030032, Shanxi, China.
  • 5 The Center for Reproductive Medicine, Department of Obstetrics and Gynaecology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China; Joint International Research Lab for Reproduction and Development, Ministry of Education, Chongqing 400010, China; Reproduction and Stem Cell Therapy Research Center of Chongqing, Chongqing 400010, China. Electronic address: dr.hefan@cqmu.edu.cn.
  • 6 The Center for Reproductive Medicine, Department of Obstetrics and Gynaecology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China; Joint International Research Lab for Reproduction and Development, Ministry of Education, Chongqing 400010, China; Reproduction and Stem Cell Therapy Research Center of Chongqing, Chongqing 400010, China. Electronic address: cqhulina@hospital.cqmu.edu.cn.
PMID: 39032906 DOI: 10.1016/j.ijbiomac.2024.133994
Abstract

Disruption of the extracellular matrix and dysregulation of the balance between Th17 and regulatory T cells are recognized as risk factors for recurrent spontaneous abortion (RSA). However, the interaction between matrix components and the Th17/Treg axis remains poorly elucidated. The result of this study revealed that the absence of type I collagen in the decidua is linked to Th17/Treg imbalance in RSA. Furthermore, we discovered that biomaterial recombinant humanized type I collagen (rhCOLI) promoted T cell differentiation into Tregs by inhibition the Notch1/Hes1 signaling pathway and enhanced the immunosuppressive function of Tregs, as indicated by increased secretion level of IL-10 and TGF-β. Importantly, this study is the first to demonstrate that rhCOLI can modulate the Th17/Treg imbalance, reduce embryo resorption rates, reshape the immune microenvironment at the maternal-fetal interface, and improve fertility in an RSA mouse model. Collectively, these findings suggest that type I collagen deficiency may contribute to, rather than result from, RSA, and propose a potential intervention for RSA using rhCOLI.

Keywords

Recombinant humanized type I collagen; Recurrent spontaneous abortion; Th17/Treg axis.

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