Transcriptional changes in the expression of chemokines related to natural killer and T regulatory cells in patients with deep infiltrative endometriosis
Natural killer and T-regulatory cells participate in the pathogenesis of endometriosis; establishing the role of certain chemokines in modulating this response represents a fundamental key to understanding the inflammatory response.
Patrick Bellelis, M.D., Denise Frediani Barbeiro, M.D., Luiz Vicente Rizzo, M.D., Ph.D., Edmund Chada Baracat, M.D., Ph.D., Mauricio Simões Abrão, M.D., Ph.D., Sergio Podgaec, M.D., Ph.D.
Volume 99, Issue 7, Pages 1987-1993, June 2013
To evaluate the expression of chemokines that regulate natural killer (NK) and T-regulatory (T-reg) cell activity in eutopic and ectopic endometrial tissue samples from endometriosis patients.
Case-control study (Canadian Task Force classification II-2).
Tertiary referral hospital.
Sixty-four consecutive patients with and without endometriosis.
After videolaparoscopy, patients were divided into three groups: bowel endometriosis (n = 22), retrocervical endometriosis (n = 10), and endometriosis-free women (n = 32).
Main Outcome Measure(s):
Gene expression of the chemokines that regulate NK (CXCL9, CXCL10, CXCL11, CXCL12, XCL1, and CX3CL1) and T-reg cell activity (CCL17 and CCL21) evaluated by real-time polymerase chain reaction.
Of the chemokines associated with NK cells, CX3CL1 and CXCL12 expression was statistically significantly greater in the foci of endometriosis compared with the eutopic endometrium in patients and controls. From the chemokines associated with T-reg cells, CCL17 expression was statistically significantly greater in the eutopic endometrium of the patients with rectosigmoid endometriosis compared with the foci of endometriosis or eutopic endometrium of the patients with retrocervical endometriosis or the disease-free women.
Both T-reg and NK cells mediate inflammatory response and may play a fundamental role in endometriosis by causing an impaired clearing of endometrial cells. Establishing how CCL17, CXCL12, and CX3CL1 modulate this response is essential to understanding inflammatory responses in endometriosis.