{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T02:44:42Z","timestamp":1790995482610,"version":"4.1.0"},"reference-count":70,"publisher":"American Society for Clinical Investigation","issue":"18","funder":[{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"crossref","award":["1071822"],"award-info":[{"award-number":["1071822"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,9,19]]},"abstract":"<jats:p>\n                    Autoimmune diseases resulting from MHC class II\u2013restricted autoantigen-specific T cell immunity include the systemic inflammatory autoimmune conditions rheumatoid arthritis and vasculitis. While currently treated with broad-acting immunosuppressive drugs, a preferable strategy is to regulate antigen-specific effector T cells (Teffs) to restore tolerance by exploiting DC antigen presentation. We targeted draining lymph node (dLN) phagocytic DCs using liposomes encapsulating 1\u03b1,25-dihydroxyvitamin D3 (calcitriol) and antigenic peptide to elucidate mechanisms of tolerance used by DCs and responding T cells under resting and immunized conditions. PD-L1 expression was upregulated in dLNs of immunized relative to naive mice. Subcutaneous administration of liposomes encapsulating OVA\n                    <jats:sub>323\u2013339<\/jats:sub>\n                    and calcitriol targeted dLN PD-L1\n                    <jats:sup>hi<\/jats:sup>\n                    DCs of immunized mice and reduced their MHC class II expression. OVA\n                    <jats:sub>323\u2013339<\/jats:sub>\n                    \/calcitriol liposomes suppressed expansion, differentiation, and function of Teffs and induced Foxp3\n                    <jats:sup>+<\/jats:sup>\n                    and IL-10\n                    <jats:sup>+<\/jats:sup>\n                    peripheral Tregs in an antigen-specific manner, which was dependent on PD-L1. Peptide\/calcitriol liposomes modulated CD40 expression by human DCs and promoted Treg induction in vitro. Liposomes encapsulating calcitriol and disease-associated peptides suppressed the severity of rheumatoid arthritis and Goodpasture\u2019s vasculitis models with suppression of antigen-specific memory T cell differentiation and function. Accordingly, peptide\/calcitriol liposomes leverage DC PD-L1 for antigen-specific T cell regulation and induce antigen-specific tolerance in inflammatory autoimmune diseases.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.126025","type":"journal-article","created":{"date-parts":[[2019,9,5]],"date-time":"2019-09-05T12:00:36Z","timestamp":1567684836000},"source":"Crossref","is-referenced-by-count":62,"title":["PD-L1\u2013 and calcitriol-dependent liposomal antigen-specific regulation of systemic inflammatory autoimmune disease"],"prefix":"10.1172","volume":"4","author":[{"given":"Ryan","family":"Galea","sequence":"first","affiliation":[{"name":"The University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Queensland, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hendrik J.","family":"Nel","sequence":"additional","affiliation":[{"name":"The University of Queensland Diamantina Institute, The University of 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