Myeloid-Derived Suppressor Cells are gaining importance in endometriosis

A milestone in the pathogenesis of endometriosis: Myeloid-Derived Suppressor Cells

Key Points

Highlights: 

• Immune modulator cells such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) may promote the progression of endometriosis.
• Major consequences of disturbed immune responses of myeloid-derived suppressor cells include immunosuppression, angiogenesis, and the release of cytokines & growth factors.

Importance:  

• The heterogeneous group of myeloid-derived suppressor cells is immature myeloid cells that include dendritic cells, granulocytes, and monocyte/macrophage precursors. 
• These cells have pathogenetic roles in the development of important human diseases such as chronic inflammation and cancer as well as endometriosis. 
• Detailed elucidation of the mechanisms underlying the immune responses by myeloid-derived suppressor cells in patients suffering from endometriosis may yield potential cure modalities.

What's done here: 

• This is a review article highlighting current research achievements regarding the elusive role of myeloid-derived suppressor cells in human diseases, in particular "endometriosis".

Key results:

• Most of the current knowledge on myeloid-derived suppressor cells is related to cancer research revealing their importance in immunosuppression, angiogenesis, the release of cytokines, or growth factors. 
• These properties of myeloid-derived suppressor cells also seem to be operative in endometriosis pathogenesis and progression.

Limitations: 

• A major drawback on the assumptions of myeloid-derived suppressor cells in endometriosis is the sparse number of scientific research projects.

Lay Summary

Dr. Wertel and associates from Polish academic centers published their sentimental review paper on the role of "Myeloid-Derived Suppressor Cells" in human diseases, in a recent issue of  Cells.

Endometriosis, the most common gynecological disease affecting about 10% of women globally, is now classified as a tumor-like lesion. In this regard, ectopic endometrial tissues outside the uterus have similarities to those of ovarian cancers with their potential of invasion, new vessel formation called neoangiogenesis, reduced cell death, and local inflammation.

Research on the subject revealed that endometriosis is associated with disturbances in immune responses, with underlying mechanisms involving disorders of neutrophils, monocytes/macrophages, dendritic cells, natural killer cells, and T lymphocytes. Additionally, in few scientific studies, immunosuppressive cells like regulatory T lymphoid cells, also called "Tregs" and myeloid-derived suppressor cells, showed that these cells are able to promote endometriosis progression.

It is now well known that both chronic inflammation and an inflammatory milieu play a significant role in endometriosis and ovarian cancer. It is an intriguing observation that both endometriosis and cancer-associated inflammation have an elevated concentration of myeloid-derived suppressor cells.

The authors suggested that understanding the pathways underlying the disturbed immune milieu of myeloid-derived suppressor cells in endometriosis may yield a starting point for inhibiting progression, and in this way preventing malignant transformation.

"It has become clearly evident that one of the major consequences of the expansion of myeloid-derived suppressor cells is immunosuppression, angiogenesis, and release of cytokines or growth factors, which may stimulate the progression of endometriosis and cancers. Taking into account their immunosuppressive activity, e.g., the ability to suppress tumor-infiltrating lymphocyte activity, increase the tumor-supportive macrophages, and regulate T lymphocyte responses, we hypothesize that they may also play an important role in the development of endometriosis-associated ovarian cancer. However, the aspect mentioned above requires further comprehensive research" they concluded.

Research Source: https://pubmed.ncbi.nlm.nih.gov/33803806/