{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T21:41:22Z","timestamp":1790890882605,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T00:00:00Z","timestamp":1785196800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T00:00:00Z","timestamp":1785196800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis &amp;amp; Rheumatology"],"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Axial spondyloarthritis (axSpA) and psoriatic arthritis (PsA) are overlapping yet distinct conditions within the SpA spectrum. As divergent immunophenotypes may influence disease course and therapeutic response, we compared immune cell subsets, cytokine profiles, and inflammatory mediators.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Peripheral blood mononuclear cells (PBMCs) from 179 patients (88 axSpA, 91 PsA) and 49 healthy donors were profiled using spectral flow cytometry, comprising 230 million acquired events and 55 million quality\u2010controlled cells. Immune subsets, activation\u2010 and differentiation\u2010associated markers, and cytokines were analyzed to define disease\u2010specific profiles.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      axSpA and PsA exhibited distinct immunophenotypic profiles. axSpA was characterized by expansion of double\u2010negative and \u03b3\u03b4 T cells, increased plasmablasts and CD21\n                      <jats:sup>low<\/jats:sup>\n                      B cells, and higher expression of activation\u2010associated markers (CD80, CD86, CD95), consistent with dysregulated innate\u2010like immune activation. PsA showed increased dendritic cells and a higher frequency of IgM\n                      <jats:sup>+<\/jats:sup>\n                      IgD\n                      <jats:sup>\u2212<\/jats:sup>\n                      memory B cells. Both diseases exhibited Th1 enrichment; however, axSpA showed additional Th17 skewing and increased expression of activation\u2010 and checkpoint\u2010associated markers (HLA\u2010DR, CD38, PD\u20101), whereas PsA displayed more central memory CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells and lower PD\u20101 expression. Cytokine profiling revealed elevated inflammasome\u2010related and innate cytokines in axSpA, whereas PsA showed increased soluble interleukin\u20102 (IL\u20102) receptor, IL\u201017A, soluble tumor necrosis factor receptor type I, and vascular\u2010associated inflammatory mediators. Regularized regression identified a stable immune signature distinguishing axSpA from PsA (cross\u2010validated area under the receiver operating characteristic curve 0.94).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>axSpA and PsA share overlapping yet distinguishable immunophenotypic signatures. axSpA shows enrichment of innate\u2010associated and broadly activated immune features, whereas PsA is characterized by adaptive and memory\u2010associated immune responses. These findings may support biomarker\u2010guided stratification within the SpA spectrum.<\/jats:p>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/art70269-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.70269","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T09:22:21Z","timestamp":1783329741000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Deep Immunophenotyping Reveals Distinct Immune Signatures in Axial Spondyloarthritis and Psoriatic Arthritis"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6415-6376","authenticated-orcid":false,"given":"Natalie","family":"Frede","sequence":"first","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Medical Center and Faculty of Medicine University of Freiburg  Freiburg im Breisgau Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nils","family":"Craig\u2010M\u00fcller","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Medical Center and Faculty of Medicine University of Freiburg  Freiburg im Breisgau Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silke","family":"Kohrt","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Medical Center and Faculty of Medicine University of Freiburg  Freiburg im Breisgau Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marei\u2010Theresa","family":"Bott","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Medical Center and Faculty of Medicine University of Freiburg  Freiburg im Breisgau Germany"},{"name":"Freeze\/IR Biobank, Faculty of Medicine University of Freiburg  Freiburg im Breisgau Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich","family":"Salzer","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Medical Center and Faculty of Medicine University of Freiburg  Freiburg im Breisgau Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana Cecilia","family":"Venhoff","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Medical Center and Faculty of Medicine University of Freiburg  Freiburg im Breisgau 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