title: The role of soluble tumor necrosis factor like weak inducer of apoptosis and interleukin-17A in the etiopathogenesis of celiac disease: A cross-sectional study.
abstract: Our aim in this study was to determine soluble tumor necrosis factor (TNF)-like weak inducer of apoptosis (sTWEAK) and interleukin-17A (IL-17A) levels in celiac disease, and their association with the gluten diet and autoantibodies. Eighty patients with celiac diagnosis and 80 healthy control individuals with similar age, gender and body mass index to the patient group were included in the study. Serum sTWEAK and IL-17A levels were measured by the serum enzyme-linked immunosorbent assay kit. The median IL-17A (117.5 pg/mL vs. 56.7 pg/mL; P = 0.001) level in celiac patients was higher than in the control group, while the median sTWEAK (543 pg/mL vs. 643 pg/mL; P = 0.016) level in patients was determined to be lower. In the patient group, patients who complied with the gluten diet had a lower level of median IL-17A (98.1 pg/mL vs. 197.5 pg/mL; P = 0.034) and a higher level of sTWEAK (606 pg/mL vs. 522.8 pg/mL; P = 0.031) than those who did not adhere. Furthermore, the IL-17A level was higher and the sTWEAK level was lower in celiac patients with positive antibody than those with negative antibody. A positive correlation was determined among anti-gliadin antibody IgA, anti-gliadin antibody IgG, anti-tissue transglutaminase IgG levels and the IL-17A level, and a negative correlation was determined with the sTWEAK level. In celiac disease, the sTWEAK and IL-17A levels differ between patients who cannot adapt to the gluten diet and who are autoantibody positive, and patients who adapt to the diet and are autoantibody negative. We believe that sTWEAK and IL-17A are associated with the inflammation in celiac pathogenesis.
authors.affiliation: aTurkey Yuksek Ihtisas Training and Research Hospital, Department of Gastroenterology bAnkara Numune Training and Research Hospital, Department of Internal Medicine cTurkey Yuksek Ihtisas Training and Research Hospital, Department of Microbiology dAtatürk Chest Diseases & Thoracic Surgery Training and Research Hospital, Department of Immunology and Allergy, Ankara, Turkey.
authors.forename: Mahmut
authors.initials: M
authors.lastname: Yuksel
authors.forename: Mustafa
authors.initials: M
authors.lastname: Kaplan
authors.forename: Ihsan
authors.initials: I
authors.lastname: Ates
authors.forename: Zeki Mesut Yaln
authors.initials: ZM
authors.lastname: Kilic
authors.forename: Hasan
authors.initials: H
authors.lastname: Kilic
authors.forename: Nuretdin
authors.initials: N
authors.lastname: Suna
authors.forename: Hale
authors.initials: H
authors.lastname: Ates
authors.forename: Ertugrul
authors.initials: E
authors.lastname: Kayacetin
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood; D002446:Celiac Disease / Q000097:blood / Q000209:etiology*; D003430:Cross-Sectional Studies; D000074049:Cytokine TWEAK; D004032:Diet; D005260:Female; D005983:Glutens; D006801:Humans; D020381:Interleukin-17 / Q000097:blood / Q000502:physiology*; D008297:Male; D048069:Tumor Necrosis Factors / Q000097:blood / Q000502:physiology*
chemical_list: D001323:Autoantibodies; D000074049:Cytokine TWEAK; C508717:IL17A protein, human; D020381:Interleukin-17; C109743:TNFSF12 protein, human; D048069:Tumor Necrosis Factors; D005983:Glutens