Skip to main content

ORIGINAL RESEARCH article

Front. Cell. Infect. Microbiol.

Sec. Clinical Infectious Diseases

Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1548238

Immune Dysregulation in Endometrial Tuberculosis: Elevated HLA-G and IL-1Ra as Key Modulators

Provisionally accepted
  • 1 Graduate School, Hebei North University, Zhangjiakou, Hebei Province, China
  • 2 Eighth Medical Center of the General Hospital of the Chinese People's Liberation Army, Beijing, Beijing, China

The final, formatted version of the article will be published soon.

    Endometrial tuberculosis (ETB) is a reproductive system infection caused by Mycobacterium tuberculosis, primarily invading the endometrium through hematogenous dissemination. This study included 10 patients diagnosed with ETB and 10 patients with pulmonary tuberculosis (PTB) to analyze their clinical, pathological, and immunological characteristics. Anatomically, PTB presented the highest prevalence among tuberculosis cases. Compared to PTB imaging, CT scans of ETB showed less distinctive diagnostic features. Pathologically, abscess formation was more frequently observed in ETB patients than in PTB patients, suggesting a more intense local inflammatory response in ETB. However, there were no statistically significant differences in granulomatous lesions, caseous necrosis, coagulative necrosis, inflammatory necrosis, exudation, acute inflammation, or fibrous tissue hyperplasia between the two groups. Immunohistochemical analysis revealed higher infiltration of macrophages (CD68) in ETB lesions compared to PTB, whereas the counts of T cells (CD3+, CD4+, CD8+) and B cells (CD20) showed no significant differences. Notably, the expression levels of HLA-G and IP-10 were significantly elevated in the lesion areas of ETB compared to PTB.Similarly, the expression of HLA-G, IP-10, IL-1Ra, and IL-10 was significantly higher in the ETB group than in the PTB group. Furthermore, HLA-G and IL-1Ra expression levels were markedly elevated in ETB lesion areas compared to surrounding normal endometrial tissue. HLA-G plays a pivotal role in immune tolerance by modulating local immune responses, while IP-10 is involved in chronic inflammatory signaling. IL-1Ra and IL-10 are key regulators of endometrial immune homeostasis, counterbalancing inflammatory responses that could otherwise disrupt reproductive function. These immunoregulatory factors are crucial in maintaining immune tolerance within the endometrium and may influence immune responses associated with endometrial tuberculosis.

    Keywords: Endometrial tuberculosis, pulmonary tuberculosis, Pathological characteristics, HLA-G, tuberculous granuloma, IL-1ra

    Received: 19 Dec 2024; Accepted: 03 Apr 2025.

    Copyright: © 2025 Huang, Dai, Yu and Chen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Haotian Yu, Eighth Medical Center of the General Hospital of the Chinese People's Liberation Army, Beijing, Beijing, China
    Wen Chen, Eighth Medical Center of the General Hospital of the Chinese People's Liberation Army, Beijing, Beijing, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

    Research integrity at Frontiers

    Man ultramarathon runner in the mountains he trains at sunset

    95% of researchers rate our articles as excellent or good

    Learn more about the work of our research integrity team to safeguard the quality of each article we publish.


    Find out more