{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T05:49:17Z","timestamp":1782452957991,"version":"3.54.5"},"reference-count":83,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T00:00:00Z","timestamp":1782432000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Cutaneous adverse drug reactions to carbamazepine range from mild maculopapular exanthema to life-threatening syndromes such as Stevens\u2013Johnson syndrome\/toxic epidermal necrolysis. While the immunological basis for HLA-B*15:02-restricted carbamazepine-induced SJS\/TEN has received greater attention, mechanisms underlying mild maculopapular exanthema remain poorly understood. In this study, we examined circulating T-cell immune recognition and transcriptomic signatures in the blood of patients with carbamazepine-induced maculopapular exanthema during active and resolved disease and compared these profiles with severe reactions. Peripheral blood was collected from patients with active (&amp;lt; 9 days post-diagnosis;\n                    <jats:italic>n<\/jats:italic>\n                    \u00a0=\u00a05) or resolved (&amp;gt; 2 months post-resolution;\n                    <jats:italic>n<\/jats:italic>\n                    \u00a0=\u00a010) carbamazepine-induced maculopapular exanthema, carbamazepine-tolerant controls (\n                    <jats:italic>n<\/jats:italic>\n                    \u00a0=\u00a011), and resolved carbamazepine-induced Stevens\u2013Johnson syndrome cases (\n                    <jats:italic>n<\/jats:italic>\n                    \u00a0=\u00a011). T-cell reactivity, T-cell receptor clonotypes, and global transcriptional profiles were assessed using cytokine assays, sequencing, and bulk RNA transcriptomics. Both active and resolved maculopapular exanthema patients exhibited polyclonal CD8\n                    <jats:sup>+<\/jats:sup>\n                    T-cell activation. Resolved cases displayed recognition of related tricyclic compounds and private CD8\n                    <jats:sup>+<\/jats:sup>\n                    T-cell receptor clonotypes. Transcriptomics revealed enrichment of complement, interferon, and CD4\n                    <jats:sup>+<\/jats:sup>\n                    T-cell-associated chemokine pathways in active disease, with persistent TNF and NF-\u03baB signalling in resolved cases. Both disease states showed reduced IGHA2 expression, indicating IgA\n                    <jats:sup>+<\/jats:sup>\n                    B-cell dysregulation. Compared with severe hypersensitivity reactions, maculopapular exanthema lacked sustained proinflammatory signalling, highlighting divergent long-term immune activation. Together, we demonstrated that carbamazepine-induced maculopapular exanthema is driven by polyclonal CD8\n                    <jats:sup>+<\/jats:sup>\n                    T-cell responses in conjunction with innate immune activation and exhibits distinct molecular signatures from severe reactions, providing mechanistic insight into the milder clinical phenotype.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1818888","type":"journal-article","created":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T05:44:22Z","timestamp":1782452662000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Immunological and molecular signatures of carbamazepine-induced maculopapular exanthema"],"prefix":"10.3389","volume":"17","author":[{"given":"Kerry A.","family":"Mullan","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Infection and Immunity Programs, Biomedicine Discovery 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L.","family":"Tucker","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Infection and Immunity Programs, Biomedicine Discovery Institute, Monash University","place":["Clayton, VIC, Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey W.","family":"Lai","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Infection and Immunity Programs, Biomedicine Discovery Institute, Monash University","place":["Clayton, VIC, Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alison","family":"Anderson","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, The University of Melbourne","place":["Melbourne, VIC, Australia"]},{"name":"Department of Neuroscience, School of Translational Medicine, Monash University","place":["Melbourne, VIC, Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marian","family":"Todaro","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, The University of Melbourne","place":["Melbourne, VIC, Australia"]},{"name":"Department of Neuroscience, School of Translational Medicine, Monash University","place":["Melbourne, VIC, Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ching-Ching","family":"Ng","sequence":"additional","affiliation":[{"name":"Institute of Biological Sciences, Faculty of Science, Universiti Malaya","place":["Kuala Lumpur, Malaysia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kheng-Seang","family":"Lim","sequence":"additional","affiliation":[{"name":"Division of Neurology, Department of Medicine, Faculty of Medicine, Universiti Malaya","place":["Kuala Lumpur, Malaysia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes 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