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作 者:彭薇 宋雅琴 韦爱萍 周秀英 温谋(综述) 谢政军(审校) PENG Wei;SONG Ya-qin;WEI Ai-ping;ZHOU Xiu-ying;WEN Mou;XIE Zheng-jun(Department of Hematology,the Fifth Affiliated Hospital of Zunyi Medical University,Zhuhai 519100,Guangdong,CHINA)
机构地区:[1]遵义医科大学第五附属(珠海)医院血液内科,广东珠海519100
出 处:《海南医学》2023年第11期1651-1655,共5页Hainan Medical Journal
基 金:遵义医科大学博士科研启动基金(编号:BS2018-01)。
摘 要:一直以来对于温抗体型自身免疫性溶血性贫血(WAIHA)发病主要环节的认识主要集中在打破自身免疫耐受的B淋巴细胞过度激活增殖,继而产生大量抗红细胞的自身抗体。近年来随着研究的深入,临床逐渐认识到在WAIHA的这一病理变化背后亦有T淋巴细胞参与其中,体现在T细胞通过共刺激信号、Ca^(2+)-NEAT、JAK-STAT、PI3K/AKT/mTOR等分子通路影响异常B淋巴细胞在抗原识别、免疫呈递、异常增殖、抗体分泌各个阶段,致使T细胞亚群在结构、数量及质量上发生失衡:Th2、Th17、Treg的过度扩增,进一步明确不同亚群T细胞在WAIHA发病中的功能状态及导致该变化的关键分子通路节点,对于复发难治型WAIHA的治疗可能带来新的治疗思路和方向。The understanding of the pathogenesis of warm autoimmune hemolytic anemia(WAIHA)has mainly focused on the excessive activation and appreciation of B lymphocytes that break the autoimmune tolerance,and then the production of a large number of anti-red cell autoantibodies.In recent years,there is growing recognition that T lym-phocytes are also involved in this pathological change in WAIHA,which is reflected in T cells affecting abnormal B lym-phocytes through costimulatory signal,Ca^(2+)-NEAT,JAK/STAT,PI3K/AKT/mTOR at various stages of antigen recogni-tion,immune presentation,abnormal proliferation,and antibody secretion,structure,quantity,and mass imbalance of T cell subsets:excessive expansion of Th2,Th17,Treg.Further clarifying the functional status of different subsets of T cells in the pathogenesis of WAIHA and the key molecular pathway nodes leading to this change may bring about new treatment ideas and directions for the treatment of relapsed and refractory WAIHA.
关 键 词:温抗体型自身免疫性溶血性贫血 自身免疫性疾病 T淋巴细胞 分子通路 免疫调控紊乱
分 类 号:R556[医药卫生—血液循环系统疾病]
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