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Published on: January 10, 2025
Abstract:
Retraction: "Impaired Th17 cell proliferation and decreased pro-inflammatory cytokine production in CXCR3/CXCR4 double-deficient mice of vulvovaginal candidiasis," by Yue-Mei Jin, Shan-Shan Liu, Tian-Min Xu, Feng-Jun Guo, Jun Chen, J Cell Physiol. 2019; 13894-13905: The above article, published online on 17 January 2019 in Wiley Online Library (https://doi.org/10.1002/jcp.28071), has been retracted by agreement between the authors, the journal's Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed after the authors stated that the experimental data in the article could not be verified. The investigation additionally revealed inconsistencies in several image elements. Thus, the editors consider the conclusions of this article to be invalid. The authors were not available for a final confirmation of the retraction.
Insights
This study on vulvovaginal candidiasis in mice is retracted due to unverified experimental data and image inconsistencies. The findings on Th17 cell proliferation and cytokine production are now considered invalid.
Area of Science:
- Immunology
- Microbiology
Context:
- Vulvovaginal candidiasis (VVC) is a common infection.
- T-helper 17 (Th17) cells and their cytokines play a role in VVC pathogenesis.
- Chemokine receptors CXCR3 and CXCR4 are involved in immune cell trafficking.
Purpose:
- To investigate the role of CXCR3 and CXCR4 in Th17 cell responses during VVC.
- To examine the impact of CXCR3/CXCR4 deficiency on pro-inflammatory cytokine production in VVC models.
Summary:
- The article investigated Th17 cell proliferation and cytokine production in CXCR3/CXCR4 double-deficient mice with vulvovaginal candidiasis.
- The study aimed to understand the role of these chemokine receptors in the immune response to Candida albicans.
- Findings suggested impaired Th17 cell function and reduced pro-inflammatory cytokines in the absence of CXCR3 and CXCR4.
Impact:
- The retraction invalidates previous conclusions regarding the specific roles of CXCR3 and CXCR4 in VVC immunity.
- This highlights the importance of data verification and reproducibility in scientific research.
- Further studies are needed to clarify the immunological mechanisms underlying VVC.
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