TIM‐3 Expression in Endometriosis
ABSTRACT Problem Endometriosis is a prevalent chronic gynecological disease linked to immune dysfunction. The protein T‐cell immunoglobulin and mucin domain‐containing protein 3 (TIM‐3) plays a crucial role in immune system balance. Malfunction of TIM‐3 may result in excessive immune activation and...
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Veröffentlicht in: | American journal of reproductive immunology (1989) 2024-06, Vol.91 (6), p.e13887-n/a |
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Zusammenfassung: | ABSTRACT
Problem
Endometriosis is a prevalent chronic gynecological disease linked to immune dysfunction. The protein T‐cell immunoglobulin and mucin domain‐containing protein 3 (TIM‐3) plays a crucial role in immune system balance. Malfunction of TIM‐3 may result in excessive immune activation and inflammatory tissue damage. Given TIM‐3's established role in the development of cancer and autoimmune diseases, we decided to study its role in women suffering from endometriosis.
Study Method
We included a total of 62 female patients, all of whom had undergone laparoscopic surgery. Of these, 47 had endometriosis and 15 did not. During surgery, we collected peritoneal fluid (PF) and peripheral blood (PB) samples from every patient for analysis using flow cytometry. To mark the samples, we used a panel of monoclonal antibodies and examined TIM‐3 expression in their immune cells.
Results
Endometriosis patients in PB demonstrated a significantly lower percentage of CD56+ T cells with TIM‐3 expression. As endometriosis progressed through its stages, this expression lessened. This decrease was particularly notable in women with stage III/IV endometriosis. Additionally, both women diagnosed with intestinal endometriosis and those with recent endometriosis diagnoses showed a significantly reduced percentage of CD56+ T cells expressing TIM‐3.
Conclusions
Patients with endometriosis exhibit diminished TIM‐3 expression within circulating T cells. This warrants further investigation to discern whether it contributes to the progression of endometriosis, potentially through the amplification of autoreactive T cells and inflammation. |
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ISSN: | 1046-7408 1600-0897 1600-0897 |
DOI: | 10.1111/aji.13887 |