Endometriosis is a common health condition among women in which tissue similar to the lining of the uterus grows outside the uterus. This condition can be found on the ovaries, fallopian tubes, and other surfaces around and outside the uterus. The presence of endometriotic tissue outside the uterus can cause pain, bleeding, infertility, and even stomach problems. It is estimated that 11% of women in the United States have endometriosis.
Immune Response
Endometriosis has previously been associated with T helper type 2 (Th2) immune responses, which are also involved in tissue repair and the progression of allergic diseases such as asthma and dermatitis. Thymic stromal lymphopoietin (TSLP) is a protein known as an alarmin that is involved in inducing Th2 responses and has been detected within endometriotic lesions. However, the role of TSLP in the pathophysiology of endometriosis was unclear.
In a recent publication in The Journal of Immunology, Stanimira Aleksieva and Dr. Chandrakant Tayade, from the Department of Biomedical and Molecular Sciences at Queen’s University, investigated the role of TSLP in the development and proliferation of endometriosis. “We found that TSLP plays a significant role in modulating the endometriotic lesion environment. TSLP is over-expressed in patient lesions, contributes to survival of endometriotic stromal cells, and promotes lesion proliferation,” said Aleksieva.
Inflammation and Endometriosis
“Our study provides evidence that TSLP induces recurrent inflammation and lesion proliferation that might result in the worsening of endometriosis, potentially leading to larger, more extensive lesions. In the long run, treatments targeting TSLP could help reduce Th2 inflammation and endometriosis lesion survival,” shared Dr. Tayade.
This work contributes to a better understanding of the mechanisms driving endometriosis which is needed for developing treatments. There is no cure for endometriosis and current treatments target symptoms but not endometriosis itself.
The research team investigated the role of TSLP in both cell lines and a mouse model. In cell lines, TSLP treatment reduced apoptosis of endometrial stromal cells and promoted the proliferation of THP-I cells, suggesting a role for TSLP in lesion development. In a mouse model of endometriosis, TSLP induced a Th2 response, modulated TSLP receptor expression in macrophages, dendritic cells, and CD4+ T cells, and increased lesion proliferation.
Future Research
Dr. Tayade and his team would like to further this research with pre-clinical studies evaluating the effects of TSLP neutralization on Th2 inflammation and endometriotic lesion development, proliferation, vascularization, and subsequent survival.
The research article is available on The Journal of Immunology website.
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