机译:TNF-α是通过肝CCL20表达的上调诱导小鼠致命自身免疫性肝炎的诱导
Center for Innovation in Immunoregulative Technology and Therapeutics Graduate School of Medicine;
Center for Innovation in Immunoregulative Technology and Therapeutics Graduate School of Medicine;
Center for Innovation in Immunoregulative Technology and Therapeutics Graduate School of Medicine;
Center for Innovation in Immunoregulative Technology and Therapeutics Graduate School of Medicine;
Center for Innovation in Immunoregulative Technology and Therapeutics Graduate School of Medicine;
Center for Innovation in Immunoregulative Technology and Therapeutics Graduate School of Medicine;
Division of Immune Regulation Institute for Genome Research University of Tokushima Tokushima;
Department of Gastroenterology and Hepatology Graduate School of Medicine Kyoto University Kyoto;
Center for Innovation in Immunoregulative Technology and Therapeutics Graduate School of Medicine;
Autoimmune hepatitis; CCL20; Mouse model; TNF-ntagonist; TNF-?;
机译:TNF-α通过上调肝CCL20表达在诱导致命的自身免疫性肝炎中至关重要
机译:TNF-α是通过肝CCL20表达的上调诱导小鼠致命自身免疫性肝炎的诱导
机译:小鼠产生IL-18的树突状细胞和肝CXCL9的表达介导自身免疫性肝炎的进展
机译:抑制丙型肝炎IRE介导的人肝细胞和小鼠中小发夹RNA的基因表达
机译:expex40L的肝脏表达的年龄依赖性增加以及ILC3对乙型肝炎病毒直接有效免疫的丰度
机译:人白细胞抗原-DR4非肥胖型糖尿病小鼠自身免疫性肝炎的诱导自身免疫性肝炎小鼠模型
机译:TNF-α通过上调肝CCL20表达在诱导致命的自身免疫性肝炎中至关重要。