1 Centre for Immunology, 107640 Westmead Institute for Medical Research , University of Sydney, New South Wales, Australia.
2 Department of Clinical Immunology and Immunopathology, ICPMR, 8539 Westmead Hospital , New South Wales, Australia.
Innate Immun. 2017 Oct;23(7):578-583. doi: 10.1177/1753425917727063. Epub 2017 Aug 24.
Mutations in the nucleotide binding domain of the PRR, NOD2, are associated with the autoinflammatory diseases Blau syndrome and early-onset sarcoidosis. Current theories suggest that constitutive activation of the NOD2 pathway may be responsible for pathogenesis of these diseases. Here, we report the phenotype of a kindred with Blau syndrome caused by a novel NOD2 mutation (p.E383D). Signaling protein and cytokine expression were examined, and the results of these experiments challenge current theories of constitutive NOD2 activation in the pathophysiology of Blau syndrome.
核苷酸结合域 PRR、NOD2 的突变与自身炎症性疾病 Blau 综合征和早发性类肉瘤病有关。目前的理论表明,NOD2 途径的组成性激活可能是这些疾病发病机制的原因。在这里,我们报告了一个由新型 NOD2 突变(p.E383D)引起的 Blau 综合征家系的表型。我们检测了信号蛋白和细胞因子的表达,这些实验结果对 Blau 综合征病理生理学中组成性 NOD2 激活的现有理论提出了挑战。