Affiliations: [a] Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran | [b] Department of Obstetrics and Gynecology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran | [c] Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
Correspondence:
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Corresponding author: Mehrnoosh Doroudchi, Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, P.O. Box: 71345-3119, Shiraz, Iran. Tel./Fax: +98 711 235 1575; E-mail: mdoroud@sums.ac.ir.
Abstract: Background:IL-17A a member of IL-17 family of cytokines is an inflammatory cytokine produced by a subset of CD4+ T cells that links innate and adaptive immunity. IL-17A has been shown to be a key mediator of inflammation in autoimmune diseases, transplant rejection and cancers. Objective:To investigate the level of IL-17A in sera of southern Iranian patients with papillary serous cystadenocarcinoma of ovary and compare it with age-matched women of the same region. Methods:In this study we investigated IL-17A and CA125 levels in sera of 26 patients with ovarian serous cystadenocarcinoma and 62 healthy age matched women by commercial ELISA assays. Results:Fifteen (58%) and 16 (61.5%) out of 26 patients showed elevated IL-17A (1.25 ± 2.25 pg/ml) and CA125 (218 ± 224.69 IU/ml) in their sera, respectively. No healthy individual had detectable IL-17A or elevated CA125 in their sera (8.85 ± 2.86 IU/ml). The mean IL-17A levels in poorly differentiated tumors (3.33 ± 2.36 pg/ml) was significantly higher than that of well differentiated (0.14 ± 0.38 pg/ml) and moderately differentiated (undetectable) tumors. There was also a positive correlation between IL-17A and CA125 in sera of patients and controls when grouped together (r=0.37, p=0.005). Conclusion:Elevation of IL-17A in a high percentage of ovarian serous cystadenocarcinoma and lack of this cytokine in healthy individuals makes it a specific candidate in diagnosis, follow up or immunotherapy.
