{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T16:10:31Z","timestamp":1784218231653,"version":"3.55.0"},"reference-count":58,"publisher":"Cold Spring Harbor Laboratory","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["RNA"],"accepted":{"date-parts":[[2026,4,26]]},"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:p>\n                    Adenosine deaminase acting on RNA 1 (ADAR1) deaminates adenosine to inosine in dsRNA. ADAR1 RNA editing marks cellular dsRNA as self, preventing aberrant activation of the antiviral dsRNA sensor MDA5.\n                    <jats:italic>Adar Ifih1<\/jats:italic>\n                    (MDA5) or\n                    <jats:italic>Adar Mavs<\/jats:italic>\n                    double mutant pups escape\n                    <jats:italic>Adar<\/jats:italic>\n                    mutant aberrant interferon induction but die early. Here, we show that long-lived\n                    <jats:italic>Adar Mavs Eif2ak2<\/jats:italic>\n                    (PKR) mice display a new residual defect: failure to maintain blood CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells due to loss of an editing-independent function of ADAR1. Further dsRNA sensor-stripping in\n                    <jats:italic>Adar Mavs Eif2ak2 Zbp1<\/jats:italic>\n                    mutants shows that loss of blood CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells is not prevented. Challenging\n                    <jats:italic>Adar<\/jats:italic>\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    heterozygous or\n                    <jats:italic>Adar Mavs Eif2ak2<\/jats:italic>\n                    mice with blood stage\n                    <jats:italic>Plasmodium yoelii<\/jats:italic>\n                    infection led to reduced parasitemia in\n                    <jats:italic>Adar<\/jats:italic>\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice by increased basal interferon. Unexpected reduced parasitemia in\n                    <jats:italic>Adar Mavs Eif2ak2<\/jats:italic>\n                    mice is also likely due to interferon-related defects specific to hematopoietic cells, leading to altered populations of \u03b3\u03b4 T cells and other immune cells. The defects observed in this partially dsRNA sensor-stripped mouse suggest that different antiviral dsRNA sensors normally complement each other.\n                  <\/jats:p>","DOI":"10.1261\/rna.081079.126","type":"journal-article","created":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T16:50:17Z","timestamp":1778259017000},"page":"1234-1256","source":"Crossref","is-referenced-by-count":0,"title":["Reconfigured immunity in\n                    <i>Adar<\/i>\n                    heterozygous and\n                    <i>Adar Mavs Eif2ak2<\/i>\n                    (PKR) triple mutant mice"],"prefix":"10.1261","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8599-3413","authenticated-orcid":false,"given":"Pavla","family":"Linhartov\u00e1","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7757-7295","authenticated-orcid":false,"given":"Jaclyn 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