Transcriptional changes in the expression of chemokines related to natural killer and T-regulatory cells in patients with deep infiltrative endometriosis  

Oleh:

Bellelis, Patrick ; Barbeiro, Denise Frediani ; Rizzo, Luiz Vicente ; Baracat, Edmund Chada ; Abrao, Mauricio Simoes

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 99 no. 07 (Jun. 2013), page 1987-1993.
Topik: Chemokines; endometriosis; endometrium; NK cells; T-regulatory cells

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2013.04 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Objective 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. Design Case-control study (Canadian Task Force classification II-2). Setting Tertiary referral hospital. Patient(s) Sixty-four consecutive patients with and without endometriosis. Intervention(s) 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. Result(s) 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. Conclusion(s) 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.

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