{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T19:23:06Z","timestamp":1782847386633,"version":"3.54.5"},"reference-count":78,"publisher":"American Society for Clinical Investigation","issue":"20","license":[{"start":{"date-parts":[[2024,10,22]],"date-time":"2024-10-22T00:00:00Z","timestamp":1729555200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National Eye Institute\/National Institutes of Health","award":["R01EY033288 (to R.D.),R01EY012963 (to R.D.),5P30EY003790 (Core Vision grant for research)."],"award-info":[{"award-number":["R01EY033288 (to R.D.),R01EY012963 (to R.D.),5P30EY003790 (Core Vision grant for research)."]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,10,22]]},"abstract":"<jats:p>\n                    After transplantation, Th1-mediated immune rejection is the predominant cause of graft failure. Th1 cell sensitization occurs through complex and context-dependent interaction among antigen-presenting cell subsets, particularly CD11b\n                    <jats:sup>+<\/jats:sup>\n                    DCs (DC2) and CD103\n                    <jats:sup>+<\/jats:sup>\n                    DCs (DC1). This interaction necessitates further investigation in the context of transplant immunity. We used well-established preclinical models of corneal transplantation and identified distinct roles of migratory CD103\n                    <jats:sup>+<\/jats:sup>\n                    DC1 in influencing the outcomes of the grafted tissue. In recipients with uninflamed corneal beds, migratory CD103\n                    <jats:sup>+<\/jats:sup>\n                    DC1 demonstrate a tolerogenic phenotype that modulates the immunogenic capacity of CD11b\n                    <jats:sup>+<\/jats:sup>\n                    DC2 primarily mediated by IL-10, suppressing alloreactive CD4\n                    <jats:sup>+<\/jats:sup>\n                    Th1 cells via the PD-L1\/PD-1 pathway and enhancing Treg-mediated tolerance via \u03b1v\u03b28 integrin\u2013activated TGF-\u03b21, thus facilitating graft survival. Conversely, in recipients with inflamed and vascularized corneal beds, IFN-\u03b3 produced by CD4\n                    <jats:sup>+<\/jats:sup>\n                    Th1 cells induced migratory CD103\n                    <jats:sup>+<\/jats:sup>\n                    DC1 to adopt an immunostimulatory phenotype, characterized by the downregulation of regulatory markers, including \u03b1v\u03b28 integrin and IL-10, and the upregulation of IL-12 and costimulatory molecules CD80\/86, resulting in graft failure. The adoptive transfer of ex vivo induced tolerogenic CD103\n                    <jats:sup>+<\/jats:sup>\n                    DC1 (iDC1) effectively inhibited Th1 polarization and preserved the tolerogenic phenotype of their physiological counterparts. Collectively, our findings underscore the essential role played by CD103\n                    <jats:sup>+<\/jats:sup>\n                    DC1 in modulating host alloimmune responses.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.182469","type":"journal-article","created":{"date-parts":[[2024,9,5]],"date-time":"2024-09-05T12:00:39Z","timestamp":1725537639000},"source":"Crossref","is-referenced-by-count":3,"title":["Acquired immunostimulatory phenotype of migratory CD103+ DCs promotes alloimmunity following corneal 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