{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T21:47:02Z","timestamp":1788990422770,"version":"build-2803163510"},"reference-count":34,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,8,19]],"date-time":"2025-08-19T00:00:00Z","timestamp":1755561600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>GM-CSF is a pro-inflammatory cytokine that promotes an inflammatory phenotype in myeloid cells. The extent and pattern of GM-CSF expression in immune cells have not been fully elucidated. Our goal was to advance this topic using novel GM-CSF reporter\/fate reporter transgenic mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We tracked ongoing and past GM-CSF expression in various immune cells from multiple organs, in steady-state and autoimmune inflammation of the central nervous system (CNS).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The GM-CSF expression patterns varied by cell type and organ, with CD4\n                      <jats:sup>+<\/jats:sup>\n                      , CD8\n                      <jats:sup>+<\/jats:sup>\n                      , and CD11b\n                      <jats:sup>+<\/jats:sup>\n                      cells being the main producers. GM-CSF expression was transient and seemingly permanently lost in most cells over time. In a mouse model of CNS autoimmunity, effector memory CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells were the dominant GM-CSF source in the CNS. A large proportion of CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells that expressed GM-CSF also expressed CXCR6, but this chemokine receptor did not play a main role in the CNS autoimmunity. Transcriptomic analysis showed notably distinct gene expression profiles between effector memory CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells that did and did not express GM-CSF.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      These findings identified distinct GM-CSF cellular sources across organs, highlighting the transient nature of GM-CSF expression and the correlation between its expression and the overall phenotype of effector memory CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells.\n                    <\/jats:p>\n                  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