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We integrated cell-specific genetic and multi-omics evidence to prioritize candidate regulatory pathways.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>cis-eQTLs from 17 immune-cell populations were integrated with RA GWAS data by two-sample Mendelian randomization. Transcriptomics, WGCNA, and machine-learning feature selection identified convergent candidates. Single-cell and virtual perturbation analyses assessed cellular localization and downstream changes. Molecular docking and dynamics computationally prioritized compounds, and knockdown\/rescue experiments evaluated the PRKCB\u2013CTSL relationship.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Eleven candidates had convergent genetic and transcriptomic support. PRKCB was retained by LASSO, SVM, and random forest and preferentially expressed in monocytes. Virtual perturbation implicated CTSL and antigen-processing\/presentation pathways. PRKCB knockdown reduced CTSL expression and NF-\u03baB phosphorylation, whereas CTSL restoration partially rescued NF-\u03baB phosphorylation. Separately, structure-based analyses computationally prioritized ursodiol for the most favorable predicted PRKCB interaction among evaluated compounds.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Genetic, transcriptomic, single-cell, computational, and in vitro evidence supports monocyte-associated PRKCB\u2013CTSL as a candidate regulatory pathway in RA. Further mechanistic and in vivo studies are required to establish its causal and pharmacological relevance.\n                      <jats:table-wrap>\n                        <jats:table>\n                          <jats:tbody>\n                            <jats:tr>\n                              <jats:td colspan=\"2\">\n                                <jats:bold>Key Points<\/jats:bold>\n                                \u2022\u00a0\n                                <jats:italic>Multi-omics analysis identified 11 key RA-associated targets.<\/jats:italic>\n                                \u2022\n                                <jats:italic>RA was classified into two molecular subtypes with distinct immune features.<\/jats:italic>\n                                \u2022\n                                <jats:italic>PRKCB was identified as the core target enriched in monocytes.<\/jats:italic>\n                                \u2022\n                                <jats:italic>The PRKCB\u2013CTSL axis may drive RA inflammation, and ursodiol showed therapeutic potential.<\/jats:italic>\n                              <\/jats:td>\n                            <\/jats:tr>\n                          <\/jats:tbody>\n                        <\/jats:table>\n                      <\/jats:table-wrap>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s10067-026-08482-4","type":"journal-article","created":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T19:42:09Z","timestamp":1792438929000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Single-cell eQTL Mendelian randomization reveals the monocyte-associated PRKCB\u2013CTSL axis as a candidate regulatory pathway and potential therapeutic target in rheumatoid arthritis"],"prefix":"10.1007","author":[{"given":"Pengli","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guohang","family":"Shen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenhua","family":"Liao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruoyan","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingjia","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nanxiang","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-8854-3598","authenticated-orcid":false,"given":"Yupei","family":"Dai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,10,19]]},"reference":[{"key":"8482_CR1","doi-asserted-by":"publisher","DOI":"10.55563\/clinexprheumatol\/4fyfje","author":"D Baeten","year":"2025","unstructured":"Baeten D et al (2025) Targeting fibroblast-like synoviocytes with CDK4\/6 inhibitors as a novel, non-immunosuppressive treatment strategy for rheumatoid arthritis. 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