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Responses may depend on both B cell and T cell activity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We performed high-dimensional mass cytometry profiling of coexisting peripheral B cell and key T cell states in treatment-na\u00efve patients and healthy individuals, and paired longitudinal samples from CPI-treated patients, with clinical annotations to define immune correlates of outcomes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>CPI-naive patients exhibited reduced CD19+ B cells, reduced B cell (CD21, IL-2, CXCR5) and T cell (CD38, CD27) activation markers, alongside enriched na\u00efve (CD21lo) and double-negative (DN2)-like B cells, CD95+IL-10+plasmablasts, consistent with extrafollicular responses. Concurrently, programmed cell death protein 1 (PD-1)+ and proliferation marker protein-67 (Ki67)+ T cell expansion indicates ongoing activation with features of proliferative exhaustion. Active disease featured increased regulatory CD95 expression on B cells and expanded T follicular helper-like and activated DN (CD4\u2212CD8\u2212) T cells, indicating sustained antigen stimulation. Pretreatment, elevated PD-1+ T cells predicted irAEs, whereas VEGF (vascular endothelial growth factor)+TGF-\u03b2 (transforming growth factor-\u03b2)+ DN\u2009T cells were enriched in patients without subsequent toxicity. Pretreatment, plasmablasts, transitional B cells, Forkhead box protein P3 (FoxP3)+ and central memory-like CD8+ T cells correlated with worse overall survival; na\u00efve CD21lo B cells, PD-1+CD8+ T cells and CD4+follicular helper-like T cells predicted shorter event-free survival; CD4+ memory\u2009T cells predicted better prognosis, implicating dysregulated differentiation and sustained activation in adverse outcomes. On-treatment, na\u00efve CD21hi B cells, plasmablasts, activated CD8+ and central memory-like CD4+ T cells expanded, indicating de novo humoral responses and cytotoxic T cell invigoration. On-treatment, increased class-switched memory (IgG2+) B and activated T cells predicted improved survival, while persistent na\u00efve and DN B cells were associated with poorer outcomes. Anti-PD-1 monotherapy expanded na\u00efve (CD21hi) B cells and global T cells. Anti-PD-1\/anti-LAG-3 (lymphocyte-activation gene 3) combination contracted memory B cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Melanoma displays aberrant peripheral B and T cell activation, maturation and exhaustion, prominent in active disease. Treatment-induced class-switched B cells and T cell invigoration predict clinical benefit and na\u00efve\/DN B cells signify resistance. Coordinated B and T cell responses, especially recurrent extrafollicular B cell and exhausted\/regulatory T cell states emerge as candidate indicators of outcome.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2026-015585","type":"journal-article","created":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T11:55:18Z","timestamp":1786103718000},"page":"e015585","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Circulating B cell and T cell activation states predict clinical outcomes in melanoma and reveal dynamic immune reinvigoration with checkpoint inhibitor immunotherapy"],"prefix":"10.1136","volume":"14","author":[{"given":"Lucy","family":"Booth","sequence":"first","affiliation":[{"name":"St. John\u2019s Institute of Dermatology, School of Basic and Medical Biosciences and KHP Centre for Translational Medicine, King\u2019s College London, Guy's Hospital, London, UK"},{"name":"Department of 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