机构地区:[1]Department of Physiology,Medical Research Center,Shenzhen University,Shenzhen,China [2]Biological Therapy Institute,Guangdong Provincial Key Laboratory of Regional Immunity and Diseases,Department of Immunology,Shenzhen University,Shenzhen,China [3]Department of Nephrology,the First Affiliated Hospital of Shenzhen University,Shenzhen,China [4]Paul L.Foster School of Medicine,Texas Tech University Health Sciences Center,El Paso,TX,USA [5]Department of Internal Medicine,Shenzhen Guangming Maternity and Child Healthcare Hospital,Shenzhen,China [6]School of Pharmaceutical Sciences,Shenzhen University,Shenzhen,China [7]Department of Biochemistry and Molecular Biology,Medical Research Center,Shenzhen University,Shenzhen,China [8]Shenzhen Key Laboratory for Systemic Aging and Intervention,National Engineering Research Center for Biotechnology(Shenzhen),Medical Research Center,Shenzhen University,Shenzhen,China [9]Department of Physiology and Pathophysiology,School of Basic Medical Sciences,Advanced Institute of Medical Sciences,Dalian Medical University,Dalian,China [10]National Clinical Research Center for Metabolic Diseases,Department of Metabolism and Endocrinology,The Second Xiangya Hospital of Central South University,Changsha,China [11]Key Laboratory of Diabetes Immunology,Ministry of Education,Changsha,China [12]Metabolic Syndrome Research Center,Clinical Immunology Center,Central South University,Changsha,China
出 处:《Cellular & Molecular Immunology》2021年第11期2530-2540,共11页中国免疫学杂志(英文版)
基 金:This work was supported by grants from the Natural Science Foundation of China(91639201,81390351,91742103 and 81770868);the Medical Scientific Research Foundation of Guangdong Province(A2020260);the Natural Science Foundation of Guangdong Province of China(2018A030313134);the Guangdong Provincial Science and Technology Program(2019B030301009);the Innovation-driven Project of CSU(2020CX015);the Shenzhen Basic Research Project(JCYJ20170818141928220,JCYJ2019073015124040376);the Shenzhen University Medical Science Cross Innovation(860000002100142).
摘 要:Immunomodulation has been considered a potential therapeutic approach for chronic kidney disease(CKD).Although it has been previously reported that CD4+T cells contribute to the development of renal fibrosis after UUO,the role of MHC class Ⅱ(MHCII)in UUO-induced renal fibrosis remains largely uncharacterized.The present study reports that the expressions of MHCII molecules in renal cortical tubules are upregulated in a mouse unilateral ureter obstruction(UUO)model.Global or renal tubule-specific ablation of MHCII significantly alleviates renal fibrosis following UUO.Additionally,renal expression of profibrotic genes showcased consistent reduction in both MHCII gene deficient mouse lines.These results demonstrate that renal tubular MHCII plays an important role in pathogenesis of renal fibrosis.
关 键 词:Chronic kidney disease Renal fibrosis MHCII Unilateral ureteral obstruction Folic acid
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