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Here, we used a tunable collagen system that models human tissue viscoelasticity to define how matrix relaxation directs dendritic cell (DC) behavior. Slow\u2010relaxing, elastic networks restrict actomyosin\u2010driven remodeling, limiting DC motility and reducing DC\u2010T cell encounters and activation. Blocking DC migration in fast\u2010relaxing matrices recapitulated key aspects of the impaired T cell priming seen in elastic networks, identifying migration as a mechanical checkpoint for immune activation. Prolonged confinement in elastic matrices induced a mechanomemory state, locking DCs into a state of reduced motility and altered chromatin accessibility. Studies using patient\u2010derived ependymoma samples confirmed these findings, establishing viscoelastic relaxation as a key physical regulator of immune priming. Together, this tunable viscoelastic platform provides a defined, human\u2010relevant model to dissect and model mechanical control of immunity for therapeutic design.<\/jats:p>","DOI":"10.1002\/adma.202523274","type":"journal-article","created":{"date-parts":[[2026,5,5]],"date-time":"2026-05-05T10:39:03Z","timestamp":1777977543000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Matrix Viscoelasticity Regulates Dendritic Cell Migration and Immune Priming"],"prefix":"10.1002","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4342-4105","authenticated-orcid":false,"given":"Wei\u2010Hung","family":"Jung","sequence":"first","affiliation":[{"name":"John A. 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