Insights on the crosstalk between dendritic cells and helper T cells in novel genetic etiology for mendelian susceptible mycobacterial disease

作     者：Emma Rey-Jurado Magdalena S.Pizarro-Ortega Alexis M.Kalergis 

作者机构：Millennium Institute on Immunology and ImmunotherapyDepartamento de Genética Molecular y MicrobiologíaFacultad de Ciencias BiológicasPontificia Universidad Católica de ChileSantiago 8330644Chile Departamento de EndocrinologíaFacultad de MedicinaPontificia Universidad Católica de ChileSantiago 8330644Chile 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)

年 卷 期：2018年第15卷第12期

页      面：1091-1094页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：This work was supported by COMISIÓN NACIONAL DE INVESTIGACIÓN CIENTÍFICA Y TECNOLÓGICA(CONICYT)FONDECYT grants N°1150862 and 3160249,The Millennium Institute on Immunology and Immunotherapy(P09/016-F) COPEC-UC Grant“Concurso Nacional de Proyectos de I+D aplicada en elámbito de los Recursos Naturales”n°2016.R.772.We also acknowledge Trinidad Cellis Donner for the support with figure design 

主　　题：mendelian susceptibility to mycobacterial disease SPPL2a deficiency cDC2 mycobacterial-specific priming IFN-γ 

摘      要：Mendelian susceptibility to mycobacterial disease(MSMD)is an inherited predisposition to infections by Bacille-Calmette Guérin(BCG)vaccine or by environmental *** etiology of MSMD has been associated with up to nineteen different genetic mutations in interferon(IFN)-γ-related genes.1 Although mycobacteria susceptibility-associated genetic mutations are rare in the population,their diagnosis is crucial for an efficient and timely *** et al.2 have recently described an autosomal recessive deficiency in the signal peptidase-like 2 A(SPPL2-a)as a new genetic etiology for MSMD in three patients that had suffered BCG dissemination disease.