Hepatology：B淋巴细胞阻止肝纤维化逆转，利于小鼠肝细胞癌的发生

2017-11-22 MedSci MedSci原创

适应性免疫通过调节炎症的固有成分、限制HSC衰老的程度来维持肝纤维化，促进HCC的发生。针对B细胞的靶向治疗可能是抗肝纤维化的有效策略。

肝细胞癌(HCC)是一种常见的肿瘤，是引起炎症相关癌症死亡的主要原因。尽管大多数HCC是由持续的炎症引起的，但是将慢性炎症与癌症发展联系起来的路径仍未完全阐明。

研究利用Mdr2-/-小鼠模型（炎症相关癌症模型）分析了适应性免疫发挥的作用。在这种情况下，适应性免疫的消除是遗传性的(Rag2-/-Mdr2-/- and muMt-Mdr2-/- mice)；或者在体内使用淋巴细胞特异性抗体(anti-CD20 or anti-CD4/CD8)消除适应性免疫的作用。

研究发现，在慢性纤维化性胆管炎中，激活的B细胞和T淋巴细胞释放促纤维化因子-α-肿瘤坏死因子（TNF-α）和其他促炎因子，这些促纤维化因子浸润Mdr2 -/ -小鼠的肝脏。在Rag2-/-Mdr2-/- and muMt-Mdr2-/-小鼠等模型，淋巴细胞消除后，抑制了肝星状细胞(HSC)活化和细胞外基质沉积，增强了肝星状细胞（HSCs）向细胞衰老的转变。此外，缺乏淋巴细胞改变了肝内代谢/氧化状态，导致巨噬细胞向抗炎M2表型极化。在Rag2-/-Mdr2-/-小鼠，肝癌的发生显著地受到抑制，与TNFalpha-NF-kappaB信号通路激活的降低有关。在Mdr2-/-小鼠，消除CD20+ B细胞，而不是CD4+/CD8+ T细胞，促进了纤维化逆转和抑制了促肿瘤基因。有趣地是，在人类HCC，B淋巴细胞的浸润，与肿瘤侵犯能力增强和无病生存率的减少有关。

适应性免疫通过调节炎症的固有成分、限制HSC衰老的程度来维持肝纤维化，促进HCC的发生。针对B细胞的靶向治疗可能是抗肝纤维化的有效策略。

原始出处：

Faggioli F， Palagano E， Di Tommaso L， et al. B lymphocytes limit senescence-driven fibrosis resolution and favor hepatocarcinogenesis in mouse liver injury. Hepatology， 2017， Nov 3. doi： 10.1002/hep.29636.

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2018-10-17 fengting15

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2018-03-24 xjy02

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2017-11-24 wetgdt

#淋巴细胞#

61 0
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2017-11-24 gwc384

#EPA#

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Hepatology：B淋巴细胞阻止肝纤维化逆转，利于小鼠肝细胞癌的发生

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