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However, the precise mechanism and molecules involved in this process remain unknown. Gene expression profiles of <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> cells from lymph node (<jats:styled-content style=\"fixed-case\">LN<\/jats:styled-content>), bone marrow (<jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content>) and peripheral blood (<jats:styled-content style=\"fixed-case\">PB<\/jats:styled-content>) indicate overexpression of a tolerogenic signature in <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> cells in lymph nodes (<jats:styled-content style=\"fixed-case\">LN<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content>). Based on their role in <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cell biology, the progression of <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content>, or immune regulation, a few genes of this 83\u2010gene signature were selected for further analyses. We observed a significant correlation between the clinical outcomes and the expression of <jats:italic><jats:styled-content style=\"fixed-case\">CAV<\/jats:styled-content>1<\/jats:italic> (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7041), <jats:italic><jats:styled-content style=\"fixed-case\">FGFR<\/jats:styled-content>1<\/jats:italic> isoform 8 (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7032), <jats:italic><jats:styled-content style=\"fixed-case\">PTPN<\/jats:styled-content>6<\/jats:italic> (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7031) and <jats:italic><jats:styled-content style=\"fixed-case\">ZWINT<\/jats:styled-content><\/jats:italic> (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b7001). <jats:italic><jats:styled-content style=\"fixed-case\">CAV<\/jats:styled-content>1,<\/jats:italic> a molecule involved in the regulation of tumour progression in other cancers, was seven\u2010fold higher in <jats:styled-content style=\"fixed-case\">LN<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> cells compared to <jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content>\u2010 and <jats:styled-content style=\"fixed-case\">PB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> cells. Knockdown of <jats:italic><jats:styled-content style=\"fixed-case\">CAV<\/jats:styled-content>1<\/jats:italic> expression in <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> cells resulted in significantly decreased migration (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7016) and proliferation (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b704). When <jats:italic><jats:styled-content style=\"fixed-case\">CAV<\/jats:styled-content>1<\/jats:italic> was knocked down in <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cell lines, we observed an inability to form immune synapses. Furthermore, <jats:italic><jats:styled-content style=\"fixed-case\">CAV<\/jats:styled-content>1<\/jats:italic> knockdown in <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> cells impaired their ability to form immune synapses with autologous <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> lymphocytes and allogeneic, healthy <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells. Subsequent analyses of microarray data showed differential expression of cytoskeletal genes, specifically those involved in actin polymerization. Therefore, we report a novel role for <jats:italic><jats:styled-content style=\"fixed-case\">CAV<\/jats:styled-content>1<\/jats:italic> in tumour\u2010induced immunosuppression during the progression of <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/j.1365-2141.2012.09148.x","type":"journal-article","created":{"date-parts":[[2012,5,10]],"date-time":"2012-05-10T10:24:44Z","timestamp":1336645484000},"page":"216-231","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Lymph node\u2010induced immune tolerance in chronic lymphocytic leukaemia: a role for caveolin\u20101"],"prefix":"10.1111","volume":"158","author":[{"given":"Christine E.","family":"Gilling","sequence":"first","affiliation":[{"name":"Department of Genetics, Cell Biology and Anatomy University of Nebraska Medical Center Omaha NE USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amit 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