盘点:2020年8月27日Blood研究精选

2020-08-30 MedSci原创 MedSci原创

2020年8月27日Blood研究精选

【1】依帕列净可纠正糖原贮积症Ib的中性粒细胞减少及其功能障碍
 
 
中性粒细胞减少和中性粒细胞功能障碍可引起糖原贮积症Ib(GSD-Ib)患者发生严重感染和炎症性肠病。近期,研究人员发现,在G6PC3缺陷的小鼠模型和两种罕见疾病(GSD-Ib和G6PC30缺乏)中,1,5-无水葡萄糖-6-磷酸积累会导致中性粒细胞减少,因而采用广泛应用的抗糖尿病药物依帕列净(一种肾葡萄糖共转运体SGLT2抑制剂)来治疗GSD-Ib。
 
4位采用粒细胞集落刺激因子(GCSF)治疗未获得完全缓解的GSD-Ib患者,在使用依帕列净治疗的一个月内,血清1,5-无水葡萄糖和中性粒细胞1,5-无水葡萄糖-6-磷酸水平军降低了。在临床上,频繁感染、粘膜病变、炎症性肠病症状均消失,且无低血糖症状。两例患者可以停用GCSF,另外两例也逐渐减少了GCSF的用量,分别减少了57%和81%。所有患者中性粒细胞数目均有所增加,而且趋于稳定。研究人员进一步证实了患者的中性粒细胞的功能也得以改善:正常的氧化爆发(3/3)、纠正的蛋白糖基化(2/2),以及正常的中性粒细胞趋化性(1/1)和杀菌活性(1/1)。
 
【2】红细胞生成调节模式新进展
 
 
促红细胞生成素(Epo)为成熟的类红细胞前体(EPs)提供主要的生存信号,且对终末促红细胞生成至关重要。尽管如此,祖细胞仍可以在Epo发挥作用之前就不可逆转地向红系分化,但如果并不需要这些祖细胞来维持红细胞(RBC)计数,那这些祖细胞就会白白浪费掉。
 
近期,研究人员确定了一种新的红细胞生成的模式化组织,并首次证明Epo前模式是通过巨核细胞信号与晚期Epo依赖性红细胞生成耦合在一起的。破坏巨核细胞的Tgfb1可通过扩大祖细胞的Epo前池使造血功能紊乱,并因此触发Epo依赖性红系前体的明显凋亡。类似地,药理阻断正常小鼠中TGFβ信号增强了Epo前模式,导致Epo敏感性EP凋亡。随后用低剂量Epo进行的治疗在两种模型中均触发了RBC的大量生产。
 
【3】胚系TET2功能丧失性突变导致儿童免疫缺陷和淋巴瘤
 
 
免疫先天缺陷的分子解剖有助于阐明个体基因的非冗余功能。研究人员招募了三名患有免疫失调综合征的儿童,这些儿童表现为易感染、淋巴结病、肝脾肿大、发育迟缓、自身免疫和B细胞或T细胞来源的淋巴瘤(B细胞的2位,T细胞的1位)。在异基因造血干细胞移植后,这三位患儿都出现了早期的自体T细胞重建。
 
通过全外显子测序,研究人员在DNA羟甲基化酶TET2中发现了罕见的、纯合的、胚系错义或无义变异。TET2可将RNA上的5-甲基胞嘧啶(5mC)催化形成5-羟甲基胞嘧啶(5hmC),在开启天然免疫反应方面具有重要功能。突变的TET2蛋白不表达或存在5-羟甲基化活性酶促缺陷,导致血液DNA整体高甲基化。在两位患儿中,循环T细胞表现出异常的免疫表型,包括双阴性细胞扩增、滤泡辅助性T细胞腔衰竭,以及Fas依赖性凋亡受损。此外,TET2缺失的B细胞表现出类开关样的重组缺陷。患儿来源的诱导多能干细胞的造血潜能向髓系细胞倾斜。
 
【4】糖皮质激素可增强FLT3抑制剂的抗FLT3突变型AML活性
 
 
FLT3是一种频发突变的基因,与急性髓系白血病(AML)的预后不良密切相关。虽然大多数AML患者最初对FLT3抑制剂治疗有反应,但最终会因耐药而复发。目前,FLT3抑制剂的耐药性产生机制以及对促进细胞存活的药物初步反应尚不清楚。
 
近期研究表明,短暂维持的药物敏感细胞亚群,即所谓的耐药持续者(DTP),可以在即使缺乏耐药性突变的情况下从细胞毒性药物暴露中存活下来。通过RNA测序和药物筛选,Gebru等发现,用选择性FLT3抑制剂奎扎替尼(quizartinib)处理FLT3-ITD AML细胞,上调了DTPs的炎症基因,从而增强了其对抗炎糖皮质激素的敏感性。在机制上,FLT3抑制剂和糖皮质激素的联合使用通过糖皮质激素依赖性受体上调促凋亡蛋白BIM和抗凋亡蛋白MCL-1的蛋白酶体降解,从而增强FLT3突变细胞的细胞死亡,且不影响野生型细胞的存活。此外,研究人员还在原发性AML患者样本和异种移植小鼠模型中证实了奎扎替尼和地塞米松联合应用时的抗白血病活性有所增强。
 

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    2020-09-01 ms6000001113694287

    学习了

    0

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    2020-08-30 ms3000000449926787

    很好

    0

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    2020-08-30 ms6000001113694287

    学习了

    0

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    2020-08-30 ms40265918001780213270

    厉害,学习到了

    0

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    2020-08-30 1461f3b1m60暂无昵称

    学习

    0

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    2020-08-30 Emdel

    厉害@#学习#

    0

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