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. 2017 Mar 13;8:274. doi: 10.3389/fimmu.2017.00274

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Copyright © 2017 Meesilpavikkai, Dik, Schrijver, Nagtzaam, van Rijswijk, Driessen, van der Spek, van Hagen and Dalm.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(A) Family pedigree of patients. Symbols in black indicate individuals with the same genetic defect and arrow signs indicate the patients enrolled in this study. (B) Table showing clinical data of all four affected individuals. (C) Sanger DNA sequencing chromatogram of mutated STAT1 gene. (D) Evolutionary conservation of p.Val653 among species. (E) Three-dimensional structure of phosphorylated STAT1 protein with the mutation (Val653Ile), the phosphorylation site (pTyr701), and the target DNA indicated.