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During treatment, a subset of patients develops a mogamulizumab\u2010associated drug rash (MAR) that is associated with a better overall survival, but underlying mechanisms remain unclear. In addition, misinterpretation of MAR as cutaneous T\u2010cell lymphoma (CTCL) progression can lead to unnecessary drug discontinuation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To conduct a comprehensive molecular characterization of MAR.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We performed single\u2010cell RNA sequencing of skin biopsies from 4 patients with MAR, compared to untreated erythrodermic CTCL (CTCL,\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20096) and healthy control (HC,\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20094) skin.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>CCR4<\/jats:italic>\n                      was primarily expressed in proliferating and non\u2010proliferating malignant T\u2010cell clones and\n                      <jats:italic>FOXP3+<\/jats:italic>\n                      regulatory T cells in untreated CTCL, which were significantly decreased in MAR. The few residual malignant clones in MAR showed retained CCR4 expression, but decreases in the central memory markers\n                      <jats:italic>SELL<\/jats:italic>\n                      and\n                      <jats:italic>CCR7<\/jats:italic>\n                      , with upregulation of the MMP2 inhibitor\n                      <jats:italic>TIMP2<\/jats:italic>\n                      and the tumour suppressor gene\n                      <jats:italic>RUNX3,<\/jats:italic>\n                      consistent with a more silenced immune phenotype. In parallel, polyclonal T cells in MAR lesions exhibited decreases in the exhaustion markers\n                      <jats:italic>TIGIT<\/jats:italic>\n                      and\n                      <jats:italic>TOX<\/jats:italic>\n                      , paralleled by upregulation of markers associated with cytotoxicity (\n                      <jats:italic>GZMA<\/jats:italic>\n                      ) and anti\u2010cancer properties (\n                      <jats:italic>ZNF683<\/jats:italic>\n                      ). This increase in tumour suppressor and cytotoxicity genes potentially reflects an anti\u2010lymphoma immune response within the MAR skin microenvironment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our study provides novel insights into the molecular properties of residual malignant clones within MAR that appear silenced, surrounded by a putatively anti\u2010tumor immune response.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jdv.70154","type":"journal-article","created":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T13:21:47Z","timestamp":1762435307000},"page":"1078-1090","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["<scp>scRNA<\/scp>\n                    \u2010Seq reveals anti\u2010lymphoma immune responses in mogamulizumab\u2010associated skin eruptions"],"prefix":"10.1111","volume":"40","author":[{"given":"Shannon","family":"Meledathu","sequence":"first","affiliation":[{"name":"Icahn School of Medicine at Mount Sinai  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agata","family":"Kurowski","sequence":"additional","affiliation":[{"name":"Icahn School of Medicine at Mount Sinai  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Malini P.","family":"Naidu","sequence":"additional","affiliation":[{"name":"Icahn School of Medicine at Mount Sinai  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonas","family":"Adalsteinsson","sequence":"additional","affiliation":[{"name":"Icahn School of Medicine at Mount Sinai  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shane A.","family":"Meehan","sequence":"additional","affiliation":[{"name":"Icahn School of Medicine at Mount Sinai  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