bims-maitce 2024-06-16 papers

Issue of 2024–06–16
two papers selected by
Andy E. Hogan, Maynooth University

Sci Adv. 2024 Jun 14. 10(24): eadn6331

MAIT cell activation and recruitment in inflammation and tissue damage in acute appendicitis.

Yichao Zheng, Fei Han, Zhengyu Wu, Bingjie Wang, Xingchi Chen, Caroline Boulouis, Yuebin Jiang, Amanda Ho, Dan He, Wan Rong Sia, Jeffrey Y W Mak, David P Fairlie, Lin-Fa Wang, Johan K Sandberg, Peter E Lobie, Shaohua Ma, Edwin Leeansyah.

Mucosal-associated invariant T (MAIT) cells are antimicrobial T cells abundant in the gut, but mechanisms for their migration into tissues during inflammation are poorly understood. Here, we used acute pediatric appendicitis (APA), a model of acute intestinal inflammation, to examine these migration mechanisms. MAIT cells were lower in numbers in circulation of patients with APA but were enriched in the inflamed appendix with increased production of proinflammatory cytokines. Using the patient-derived appendix organoid (PDAO) model, we found that circulating MAIT cells treated with inflammatory cytokines elevated in APA up-regulated chemokine receptors, including CCR1, CCR3, and CCR4. They exhibited enhanced infiltration of Escherichia coli-pulsed PDAO in a CCR1-, CCR2-, and CCR4-dependent manner. Close interactions of MAIT cells with infected organoids led to the PDAO structural destruction and death. These findings reveal a previously unidentified mechanism of MAIT cell tissue homing, their participation in tissue damage in APA, and their intricate relationship with mucosal tissues during acute intestinal inflammation in humans.

DOI: https://doi.org/10.1126/sciadv.adn6331

Int J Reprod Biomed. 2023 Mar;22(3): 235-244

Human V α 7.2-J α 33 mucosal-associated invariant T cells in endometrial ectopic tissues tend to produce interferon-gamma: A new player in endometriosis etiology: A case-control study.

Maryam Zare Moghaddam, Fateme Zare, Reyhane Sandoghsaz, Abbas Khalili, Ali Shams.

Background: Endometriosis is a chronic estrogen-related inflammatory disorder that is known by proliferating endometrial cells in a place outside the uterus. The high presence of immune cells in the peritoneal fluid of women with endometriosis confirms the involvement of the immune system in the pathogenesis of the disease. Mucosal-associated invariant T (MAIT) cells play an undeniable impact on mucosal immunity by the production of interleukin-17, interferon-gamma (IFN-γ), and tumor necrosis factor-alpha. The function of the cells in the pathogenesis of endometriosis is less investigated.
Objective: This study aims to investigate the infiltration of MAIT cells by using the determination levels of V α 7.2-J α 33 gene expression in eutopic and ectopic tissue of endometriosis lesions.
Materials and Methods: In this case-control study, the tested samples include 20 eutopic and 20 ectopic tissues of women with endometriosis and 20 uterine endometrial tissues of women in the control group. Expressions of the V α 7.2-J α 33 tumor necrosis factor-alpha, interleukin-17A, and IFN-γ genes were analyzed by quantitative reverse transcriptase-polymerase chain reaction.
Results: According to the results, V α 7.2-J α 33 gene expression did not show substantial elevation in the uterine and eutopic endometrial tissues compared to internal gene control as well as in ectopic tissues. Correlation analysis approved a positive relationship between V α 7.2-J α 33 expression genes and IFN-γ levels in ectopic tissues.
Conclusion: Considering the low-expression specific gene of MAIT cells in ectopic tissue, it can be concluded that these cells are present in the endometriotic environment to a certain extent, and there is a possibility of their role in the progression of endometriosis by secreting IFN- γ .

Keywords: Endometriosis, MAIT, IFN-γ, TNF-α; IL-17.; TCR V alpha 7.2-J alpha33

DOI: https://doi.org/10.18502/ijrm.v22i3.16168