Anti-IL17F Monoclonal antibody, clone TIMS28

Purpose: To investigate the associations of IL17A, IL17F, IL23A, and IL23R copy number variants (CNVs) with Vogt-Koyanagi-Harada (VKH) syndrome and Behcet's disease (BD) and the possible mechanisms involved. Design: Two-stage case-control and functional studies. Participants: A total of 1159 VKH patients, 1036 BD patients, and 2050 controls were enrolled. Methods: TaqMan real-time polymerase chain reaction assay was used for genotyping of copy number variant. Cell proliferation was measured by colorimetric assay. Main Outcome Measures: Association of CNVs in IL17A, IL17F, IL23A, and IL23R with BD and VKH syndrome and the functional roles of IL17F CNVs. Results: Increased frequencies of more than 2 copies of IL17F and IL23A were found in BD patients as compared with controls (IL17F: P = 4.17 x 10(-8); odds ratio [OR], 2.2; IL23A: P = 2.86 x 10(-11); OR, 2.8, respectively). A similar result was found for VKH syndrome (IL17F: P = 2.84 x 10(-13); OR, 2.7; IL23A: P = 4.46 x 10(-17); OR, 3.4, respectively). Interestingly, the association of IL17F and IL23A with BD was found only in male patients (IL17F: P = 1.06 x 10(-6); OR, 2.3; IL23A, P = 3.81 x 10(-8); OR, 2.8, respectively), but not in female patients. No association of CNVs in IL17A and IL23R was found for BD and VKH syndrome. IL17F protein levels were correlated positively with gene copy numbers (P = 3.43 x 10(-7)). Individuals with high IL17F copies showed enhanced peripheral blood mononuclear cells (PBMC) proliferation (P = 5.67 x 10(-3)). Conclusions: High gene copy numbers of IL17F and IL23A were associated with BD and VKH syndrome. Enhanced IL17F protein production and PBMC proliferation were associated with high IL17F copy numbers. (C) 2015 by the American Academy of Ophthalmology.

Objective: Vitiligo is a disorder of pigmentation characterized by the presence of depigmented skin macules due to a chronic and progressive loss of melanocytes from the cutaneous epidermis. Among many different etiologic hypotheses that have been suggested so far for vitiligo, the most compelling one involves a combination of environmental and genetic factors that cause autoimmune melanocyte destruction. The purpose of this study is then to determine whether there is any relationship between vitiligo and IL17 gene Glu126Gly, His161Arg and G197A polymorphisms. Design: Controlled prospective study Setting: Department of Molecular Biology and Genetics, Bulent Ecevit University Subjects: Genetic polymorphisms of IL17 gene were detected by using polymerase chain reaction based restriction fragment length polymorphism in 86 vitiligo patients and 90 healthy controls. Intervention: For genetic analysis, 5 ml of venous blood was drawn into tubes containing EDTA from each patient. Main outcome measures: IL17 gene Glu126Gly, His161Arg and G197A polymorphisms in vitiligo patients Results: As a result of our study, we have found a significant relation between His161Arg polymorphism of IL17F gene and vitiligo patients (p = 0.045). Conclusions: Our findings suggest that the IL17F His161Arg gene polymorphism has a protective role in susceptibility to vitiligo. This may be regarded as hypothesis-generating and should further be investigated in independent studies.