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Many genome-wide association studies (GWAS) have reported that numerous genetic loci were significantly associated with PBC susceptibility. However, the effects of genetic determinants on liver cells and its immune microenvironment for PBC remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We constructed a powerful computational framework to integrate GWAS summary statistics with scRNA-seq data to uncover genetics-modulated liver cell subpopulations for PBC. Based on our multi-omics integrative analysis, 29 risk genes including\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      ,\n                      <jats:italic>GSNK2B<\/jats:italic>\n                      , and\n                      <jats:italic>DDAH2<\/jats:italic>\n                      were significantly associated with PBC susceptibility. By combining GWAS summary statistics with scRNA-seq data, we found that cholangiocytes exhibited a notable enrichment by PBC-related genetic association signals (Permuted P\u2009&lt;\u20090.05). The risk gene of\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      showed the highest expression proportion in cholangiocytes than other liver cells (22.38%). The\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      cholangiocytes have prominently higher metabolism activity score than\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      cholangiocytes (P\u2009=\u20091.38\u2009\u00d7\u200910\n                      <jats:sup>\u201315<\/jats:sup>\n                      ). Compared with\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      cholangiocytes, there were 77 significantly differentially expressed genes among\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      cholangiocytes (FDR\u2009&lt;\u20090.05), and these significant genes were associated with autoimmune diseases-related functional terms or pathways. The\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      cholangiocytes exhibited relatively high communications with macrophage and monocyte. Compared with\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      cholangiocytes, the VEGF signaling pathway is specific for\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      cholangiocytes to interact with other cell populations.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      To the best of our knowledge, this is the first study to integrate genetic information with single cell sequencing data for parsing genetics-influenced liver cells for PBC risk. We identified that\n                      <jats:italic>ORMDL3<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      cholangiocytes with higher metabolism activity play important immune-modulatory roles in the etiology of PBC.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical Abstract<\/jats:title>\n                  <\/jats:sec>","DOI":"10.1186\/s12951-021-01154-2","type":"journal-article","created":{"date-parts":[[2021,12,6]],"date-time":"2021-12-06T06:05:59Z","timestamp":1638770759000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Single cell sequencing analysis identifies genetics-modulated ORMDL3+ cholangiocytes having higher metabolic effects on primary biliary cholangitis"],"prefix":"10.1186","volume":"19","author":[{"given":"Bingyu","family":"Xiang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chunyu","family":"Deng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fei","family":"Qiu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingjing","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shanshan","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huifang","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiuli","family":"Lin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yukuan","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yijun","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianzhong","family":"Su","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingqin","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1299-4802","authenticated-orcid":false,"given":"Yunlong","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,12,6]]},"reference":[{"issue":"5","key":"1154_CR1","doi-asserted-by":"publisher","first-page":"1285","DOI":"10.1016\/j.jhep.2015.06.031","volume":"63","author":"U Beuers","year":"2015","unstructured":"Beuers U, Gershwin ME, Gish RG, Invernizzi P, Jones DE, Lindor K, Ma X, Mackay IR, Par\u00e9s A, Tanaka A, et al. 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