Commentary on“Desialylated Platelets Maintain Immune Quiescence through Regulating Kupffer Cells”  

作　　者：Chen Li Craig N.Morrell 

机构地区：[1]Aab Cardiovascular Research Institute,University of Rochester School of Medicine and Dentistry,Rochester,NY,USA [2]Department of Pharmacology and Physiology,University of Rochester School of Medicine and Dentistry,Rochester,NY,USA [3]Department of Medicine,University of Rochester School of Medicine and Dentistry,Rochester,NY,USA [4]Department of Microbiology and Immunology,University of Rochester School of Medicine and Dentistry,Rochester,NY,USA [5]Department of Pathology and Laboratory Medicine,University of Rochester School of Medicine and Dentistry,Rochester,NY,USA.

出　　处：《Research》2024年第3期621-623,共3页研究（英文）

摘　　要：Platelets have long been studied for their roles in hemostasis and vascular injury repair. However, there is a continually evolving and deepening understanding that platelets initiate and regulate responses to tissue injury and pathogens, leading to platelets now being considered immune modulatory cells [1]. Platelets actively participate in host immune responses directly through pathogen engulfing and killing, or by regulating both innate and adaptive immune responses to infection or tissue injury [2]. Activated platelets promote inflammatory responses to tissue injury or infection by direct contact dependent interactions with immune cells and through indirect interactions via released soluble factors. However, mice that are deficient in platelets have skewed T helper cell differentiation [3] and increased vascular permeability [4], implying poorly defined roles for platelets in maintaining healthy immune homeostasis.

关 键 词：PLATELET homeostasis IMMUNE 

分 类 号：R54[医药卫生—心血管疾病]