{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,11]],"date-time":"2026-10-11T02:22:19Z","timestamp":1791685339655,"version":"4.3.4"},"reference-count":41,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2025,8,25]],"date-time":"2025-08-25T00:00:00Z","timestamp":1756080000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft DFG","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017694","name":"Hermann and Lilly Schilling Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100017694","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Centre for Healthy Ageing (CHA) Mainz"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,1,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Pro-inflammatory T-helper 17 (Th17) cells are of vital importance in human autoimmune diseases such as multiple sclerosis (MS). Due to differentiation and functional plasticity, Th17 cells are able to produce a variety of pro-inflammatory cytokines such as interleukin (IL)-17A, interferon (IFN)-\u03b3 and granulocyte-macrophage colony-stimulating factor (GM-CSF), and modulation of Th17 cell activities represents a desirable tool for disease-modifying treatment. Here, we aimed to understand the role of the surface molecule CD5 and its intracellular interaction partner casein kinase 2 (CK2) in human Th17 effector function as well as their role in multiple sclerosis.<\/jats:p>\n                  <jats:p>We performed targeted single-cell RNA sequencing from CSF obtained from people with multiple sclerosis and non-inflammatory neurological diseases, and high-sensitivity proteomic analysis of serum and CSF from 114 people with multiple sclerosis by using a proximity extension assay (PEA) together with functional investigations on CD4+ memory T cells differentiated into a Th17-polarized phenotype.<\/jats:p>\n                  <jats:p>Blockade of CD5 reduced the production of IL-17A, IFN-\u03b3 and GM-CSF by Th17-polarized cells without affecting proliferation. In comparison, blockade of its intracellular interaction partner CK2 exerted partly similar effects with a decrease in IL-17A and GM-CSF production but also impaired T cell proliferation. Both blocking agents resulted in a decreased phosphorylation of the downstream signalling molecule STAT3. The CD5 targeting treatment was able to abolish cytotoxic effects caused by Th17-polarized cells. Importantly, transcriptomic and proteomic analysis showed that CD5 expression correlates with an inflammatory immune profile in multiple sclerosis in serum as well as CSF.<\/jats:p>\n                  <jats:p>Our study highlights the importance of the CD5-CK2-STAT3 signalling axis for inflammatory responses of human Th17-polarized cells. Since in humans CD5 expression correlates with inflammation and cellular injury, targeting the CD5 signalling pathway provides future therapeutic opportunities for\u2014among other diseases\u2014multiple sclerosis.<\/jats:p>","DOI":"10.1093\/brain\/awaf268","type":"journal-article","created":{"date-parts":[[2025,8,22]],"date-time":"2025-08-22T11:42:54Z","timestamp":1755862974000},"page":"123-133","source":"Crossref","is-referenced-by-count":6,"title":["Role of CD5 signalling for pro-inflammatory Th17 response in multiple sclerosis"],"prefix":"10.1093","volume":"149","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9211-5873","authenticated-orcid":false,"given":"Katrin","family":"Pape","sequence":"first","affiliation":[{"name":"Department of Neurology, Research Center for Immunotherapy (FZI) and Focus Program Translational Neuroscience (FTN), University Medical Center of the Johannes Gutenberg University Mainz , Mainz 55131 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Center of the Johannes Gutenberg University Mainz , Mainz 55131 ,","place":["Germany"]},{"name":"German Cancer Consortium (DKTK) , Heidelberg D-69120 ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tobias","family":"Bopp","sequence":"additional","affiliation":[{"name":"Institute for Immunology, Research Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg University Mainz , Mainz 55131 ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2179-3655","authenticated-orcid":false,"given":"Stefan","family":"Bittner","sequence":"additional","affiliation":[{"name":"Department of Neurology, Research Center for Immunotherapy (FZI) and Focus Program Translational Neuroscience (FTN), University Medical Center of the Johannes Gutenberg University Mainz , Mainz 55131 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