{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T06:46:47Z","timestamp":1791269207534,"version":"4.1.0"},"reference-count":36,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2015,3,1]],"date-time":"2015-03-01T00:00:00Z","timestamp":1425168000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Interferon &amp; Cytokine Research"],"published-print":{"date-parts":[[2015,3]]},"abstract":"<jats:p>\n                    Adaptor protein-3 (AP-3) is a heterotetrameric complex, which regulates vesicular trafficking. Mutations of the \u03b23A subunit cause the Hermansky\u2013Pudlak syndrome type 2 (HPS-2), a rare genetic disease characterized by albinism, platelet defects, and recurrent infections. Likewise,\n                    <jats:italic toggle=\"yes\">pearl<\/jats:italic>\n                    mice, which lack functional AP-3, show several HPS-2 defects. The AP-3 absence results in defective toll-like receptor trafficking and signaling in dendritic cells (DC), but its effect on the efficiency of the\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    antiviral response is unclear. We evaluated the impact of AP-3 deficiency on the distribution of DC subsets, interferon (IFN) production, and the susceptibility to murine cytomegalovirus (MCMV) infection.\n                    <jats:italic toggle=\"yes\">Pearl<\/jats:italic>\n                    mice showed a distribution and frequency of conventional (cDC) and plasmacytoid DC (pDC) similar to that of wild-type mice both before and after MCMV infection. Moreover,\n                    <jats:italic toggle=\"yes\">pearl<\/jats:italic>\n                    mice controlled MCMV infection even at high virus doses and showed a normal production of IFN-\u03b1. Since pDC, but not cDC, from\n                    <jats:italic toggle=\"yes\">pearl<\/jats:italic>\n                    mice showed an impaired IFN-\u03b1 and tumor necrosis factor-\u03b1 production in response to prototypic DNA (MCMV and\n                    <jats:italic toggle=\"yes\">Herpes Simplex<\/jats:italic>\n                    virus) or RNA (\n                    <jats:italic toggle=\"yes\">Vesicular Stomatitis<\/jats:italic>\n                    virus) viruses\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    , it is likely that MCMV infection can be controlled\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    independently of an efficient production of IFN-\u03b1 by pDC, and that the AP-3 complex has a minimal impact on protective antiviral responses.\n                  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