Another Study Suggesting That Endometriosis May Be a Disease Associated With Immune System Dysfunction


Another Study Suggesting That Endometriosis May Be a Disease Associated With Immune System Dysfunction

The immune system protein TGF-β may be creating an environment favorable for the formation of ectopic lesions in the pelvic cavity.

Key Points

Highlights:

  • The immune system protein TGF-β may be promoting the development of endometriosis by creating an environment favorable for the development of ectopic lesions

Importance:

  • This finding supports the idea that endometriosis may be, at least in part, a disease associated with immune dysfunction.
  • This knowledge can help researchers develop new ways to manage the condition.

What's done here:

  • Researchers analyzed the peritoneal fluid and blood of 51 women with and 15 women without endometriosis.

Key results:

  • TGF-β1, TGF-β2, TGF-β3 were increased in the peritoneal fluid and blood of women with endometriosis compared to women without the disease.
  • The biggest increase was measured in the case of TGF-β1. 
  • Higher levels of IL-1β, IL-6, IL-10, and IL-17 were observed in the peritoneal fluid and blood of women with endometriosis compared to those without the disease. 
  • The studied parameters were found at higher levels in the peritoneal fluid compared to blood.

Limitations:

The study included a relatively small number of women and more research is needed to confirm these findings.

Lay Summary

An immune system protein called TGF-β in the peritoneal fluid or fluid that lubricates the lining of the abdominal wall and pelvic cavity may be creating an environment favorable for the formation of endometrial lesions. This is according to a study published in the scientific journal Immunology Letters

This finding is important because it supports the idea that endometriosis may be, at least in part, a disease associated with immune system dysfunction.

Researchers proposed several causes for the development of endometriosis but they have not been able to identify a single causative factor. Instead, the disease seems to be the result of many different factors from genetics to lifestyle and immune system dysfunction.

The deregulated activity of TGF-β, a major immune factor that plays a role in regulating cell proliferation, differentiation, new blood vessel formation, and immune responses, is known to be implicated in the pathogenesis of endometriosis.

In the present study, researchers led by Dr. ZdzisławaKondera-Anasz at the Medical University of Silesia in Katowice, Poland shed light on the mechanism through which TGF-β may be promoting the development of endometriosis. 

They showed that TGF-β could be affecting the differentiation of immune cells called T helper cells into T helper 17 or regulatory T cells. T helper 17 cells produce inflammatory factors such as  IL-17 A, IL-17 F, IL-22, and IL-21. Regulatory T cells are involved in immune suppression. Therefore, by affecting the differentiation of T helpers cells, TGF-β may be promoting the production of more factors that trigger inflammation in the peritoneal fluid and have an indirect influence on inflammation.

The researchers analyzed a total of 66 women of reproductive age, 51 of whom had endometriosis and 15 did not, serving as controls. They measured the levels of several cell singling molecules in the peritoneal fluid and blood of the women.

They found that the levels of TGF-β1, TGF-β2, TGF-β3 were increased in the peritoneal fluid and blood of women with endometriosis compared to those without the disease. They observed the biggest increase in the case of TGF-β1. 

In addition, they observed higher levels of IL-1β, IL-6, IL-10, and IL-17 in the peritoneal fluid and blood of women with endometriosis compared to women without the disease. They found that all factors they looked at were higher in the peritoneal fluid compared to the blood.

 

“TGF-β in peritoneal fluid may promote an environment favorable to ectopic lesion formation,” they concluded.


Research Source: https://www.ncbi.nlm.nih.gov/pubmed/30367890


TGF-? immune system

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