An open-label trial of JAK 1/2 blockade in progressive IFIH1-associated neuroinflammation
暂无分享,去创建一个
Y. Crow | G. Rice | K. Kothur | R. Dale | P. Brogan | S. Bandodkar | L. Wienholt | P. Barclay | Alexandra M. Johnson | S. Chu
[1] F. Rieux-Laucat,et al. Efficacy of the Janus kinase 1/2 inhibitor ruxolitinib in the treatment of vasculopathy associated with TMEM173-activating mutations in 3 children. , 2016, The Journal of allergy and clinical immunology.
[2] Y. Crow,et al. Type I interferon–mediated monogenic autoinflammation: The type I interferonopathies, a conceptual overview , 2016, The Journal of experimental medicine.
[3] E. Tantsis,et al. B Cell, Th17, and Neutrophil Related Cerebrospinal Fluid Cytokine/Chemokines Are Elevated in MOG Antibody Associated Demyelination , 2016, PloS one.
[4] O. Ohara,et al. Aicardi-Goutières syndrome is caused by IFIH1 mutations. , 2014, American journal of human genetics.
[5] L. Lagae,et al. Gain-of-function mutations in IFIH1 cause a spectrum of human disease phenotypes associated with upregulated type I interferon signaling , 2014, Nature Genetics.
[6] A. Vanderver,et al. Assessment of interferon-related biomarkers in Aicardi-Goutières syndrome associated with mutations in TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, and ADAR: a case-control study , 2013, The Lancet Neurology.
[7] A. Tefferi,et al. Serious adverse events during ruxolitinib treatment discontinuation in patients with myelofibrosis. , 2011, Mayo Clinic proceedings.