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IL-24 producing regulatory T and B lymphocytes in endometriosis
Anna Ewa Kedzierska1, Daria Lorek2, Anna Slawek1
1Department of Experimental Therapy, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.
Insights
Regulatory T (Tregs) and B lymphocytes (Bregs) produce IL-24 in endometriosis patients. Their percentages are altered, potentially enhancing immunosuppression and lesion growth.
Area of Science:
- Immunology
- Reproductive Biology
- Cytokine Signaling
Background:
- Endometriosis is characterized by an imbalance of pro- and anti-inflammatory cytokines.
- Interleukin-24 (IL-24) is a pleiotropic cytokine with diverse cellular sources.
- IL-24 expression in regulatory T cells (Tregs) and regulatory B cells (Bregs) in endometriosis remains unexplored.
Purpose of the Study:
- To investigate the expression of IL-24 in Tregs and specific Breg subpopulations in women with endometriosis compared to healthy controls.
- To determine if IL-24 production by these regulatory cells is altered in endometriosis.
Main Methods:
- Peripheral blood samples were collected from women with endometriosis (n=24) and healthy women (n=24).
- Flow cytometry was used to quantify percentages of IL-24-producing Tregs, B10 cells, immature B cells, and plasmablasts.
Main Results:
- Increased percentages of IL-24-producing Tregs were observed in women with endometriosis, particularly in stages III and IV.
- Higher percentages of IL-24-producing plasmablasts were found in the overall endometriosis cohort and stage IV.
- Conversely, IL-24-producing immature B cells were lower in the endometriosis group.
Conclusions:
- This study demonstrates for the first time that Tregs and Bregs secrete IL-24, with altered percentages in endometriosis.
- The functional significance of IL-24 secretion by regulatory cells in endometriosis is currently unclear.
- It is hypothesized that IL-24 may contribute to enhanced immunosuppressive activity, facilitating endometrial lesion growth.
Problem:
Unbalanced production of pro- and anti-inflammatory cytokines by immune cells is a hallmark of endometriosis. IL-24, a member of the IL-10 family, is a pleiotropic cytokine produced by both non-immune cells like astrocytes, keratinocytes, pancreatic myofibroblasts, and endothelial cells and immune cells such as monocytes, macrophages, dendritic cells, NK cells, T cells (including Th2 and Th17), and B cells. However, its expression in regulatory T (Tregs) and B lymphocytes (Bregs) has not been explored. In this study, we determined the expression of IL-24 in Tregs and selected Breg subpopulations in women with endometriosis compared with healthy women.
Methods:
Percentages of Tregs, B10 cells, immature B cells, and plasmablasts that produce IL-24 were measured in the peripheral blood of women with endometriosis (n=24) and healthy women (n=24) using flow cytometry.
Results:
We observed an increased percentage of IL-24-producing Tregs in the total pool of women with endometriosis and in women with stages III and IV of endometriosis compared to controls. Within the Breg subpopulations, the percentages of IL-24-producing plasmablasts were higher in the overall endometriosis cohort as well as in women with stage IV endometriosis compared with healthy women. In contrast, the percentages of IL-24-producing immature B cells were lower in the endometriosis group than that in the control group.
Conclusions:
We have shown, for the first time, that Tregs and Bregs secrete IL-24 and that their percentages are altered in endometriosis. The significance of this cytokine secretion by regulatory cells is unclear, but we speculated that IL-24 may enhance the improper immunosuppressive activity of Tregs and plasmablasts in endometriosis, which enables the implantation and growth of endometrial lesions outside the uterus.
