| Literature DB >> 33248023 |
Jun Wang1, Yanhui Xu1, Zhanghua Chen2, Jiankun Liang1, Zefeng Lin1, Huiying Liang1, Yiping Xu1, Qi Wu1, Xuanjie Guo1, Junli Nie1, Bingtai Lu1, Bing Huang1, Huifang Xian1, Xiaohui Wang3, Qiang Wu1, Jixiao Zeng1, Chengwei Chai1, Meixue Zhang1, Yuzhen Lin1, Li Zhang1, Shanmeizi Zhao1, Yanlu Tong1, Liang Zeng1, Xiaoqiong Gu1, Zhuang-Gui Chen4, Shuhong Yi4, Tong Zhang4, David Delfouneso1, Yan Zhang1, Stephen L Nutt5, Andrew M Lew5, Liwei Lu3, Fan Bai6, Huimin Xia7, Zhe Wen8, Yuxia Zhang9.
Abstract
Biliary atresia (BA) is a severe cholangiopathy that leads to liver failure in infants, but its pathogenesis remains to be fully characterized. By single-cell RNA profiling, we observed macrophage hypo-inflammation, Kupffer cell scavenger function defects, cytotoxic T cell expansion, and deficiency of CX3CR1+effector T and natural killer (NK) cells in infants with BA. More importantly, we discovered that hepatic B cell lymphopoiesis did not cease after birth and that tolerance defects contributed to immunoglobulin G (IgG)-autoantibody accumulation in BA. In a rhesus-rotavirus induced BA model, depleting B cells or blocking antigen presentation ameliorated liver damage. In a pilot clinical study, we demonstrated that rituximab was effective in depleting hepatic B cells and restoring the functions of macrophages, Kupffer cells, and T cells to levels comparable to those of control subjects. In summary, our comprehensive immune profiling in infants with BA had educed that B-cell-modifying therapies may alleviate liver pathology.Entities:
Keywords: B cell haematopoiesis; CX3CR1; Rituximab; TNFSF13B; autoantibody; biliary atresia; cytotoxicity; hypo-inflammation; scRNA-seq
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Year: 2020 PMID: 33248023 DOI: 10.1016/j.cell.2020.10.048
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582