{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T07:52:58Z","timestamp":1793087578296,"version":"4.5.0"},"reference-count":81,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2014,12,1]],"date-time":"2014-12-01T00:00:00Z","timestamp":1417392000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,12,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Localized upregulation of type I IFN was previously implicated in development of Borrelia burgdorferi\u2013induced arthritis in C3H mice, and was remarkable due to its absence in the mildly arthritic C57BL\/6 (B6) mice. Independently, forward genetics analysis identified a quantitative trait locus on Chr4, termed B. burgdorferi\u2013associated locus 1 (Bbaa1), that regulates Lyme arthritis severity and includes the 15 type I IFN genes. Involvement of Bbaa1 in arthritis development was confirmed in B6 mice congenic for the C3H allele of Bbaa1 (B6.C3-Bbaa1), which developed more severe Lyme arthritis and K\/B\u00d7N model of rheumatoid arthritis (RA) than did parental B6 mice. Administration of a type I IFN receptor blocking mAb reduced the severity of both Lyme arthritis and RA in B6.C3-Bbaa1 mice, formally linking genetic elements within Bbaa1 to pathological production of type I IFN. Bone marrow\u2013derived macrophages from Bbaa1 congenic mice implicated this locus as a regulator of type I IFN induction and downstream target gene expression. Bbaa1-mediated regulation of IFN-inducible genes was upstream of IFN receptor\u2013dependent amplification; however, the overall magnitude of the response was dependent on autocrine\/paracrine responses to IFN-\u03b2. In addition, the Bbaa1 locus modulated the functional phenotype ascribed to bone marrow\u2013derived macrophages: the B6 allele promoted expression of M2 markers, whereas the C3H allele promoted induction of M1 responses. This report identifies a genetic locus physically and functionally linked to type I IFN that contributes to the pathogenesis of both Lyme and RA.<\/jats:p>","DOI":"10.4049\/jimmunol.1401746","type":"journal-article","created":{"date-parts":[[2014,11,7]],"date-time":"2014-11-07T08:39:57Z","timestamp":1415349597000},"page":"6050-6060","source":"Crossref","is-referenced-by-count":28,"title":["<i>Borrelia burgdorferi<\/i> Arthritis\u2013Associated Locus <i>Bbaa1<\/i> Regulates Lyme Arthritis and K\/B\u00d7N Serum Transfer Arthritis through Intrinsic Control of Type I IFN Production"],"prefix":"10.1093","volume":"193","author":[{"given":"Ying","family":"Ma","sequence":"first","affiliation":[{"name":"Division of Microbiology and Immunology, Department of Pathology, University of Utah , Salt Lake City, UT 84112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenneth K C","family":"Bramwell","sequence":"additional","affiliation":[{"name":"Division of Microbiology and Immunology, Department of Pathology, University of Utah , Salt Lake City, UT 84112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert B","family":"Lochhead","sequence":"additional","affiliation":[{"name":"Division of Microbiology and Immunology, Department of Pathology, University of Utah , Salt Lake City, UT 84112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jackie K","family":"Paquette","sequence":"additional","affiliation":[{"name":"Division of Microbiology and Immunology, Department of Pathology, University of Utah , Salt Lake City, UT 84112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James F","family":"Zachary","sequence":"additional","affiliation":[{"name":"Department of Veterinary Pathobiology, University of Illinois at Urbana-Champaign , Urbana, IL 61802"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John H","family":"Weis","sequence":"additional","affiliation":[{"name":"Division of Microbiology and Immunology, Department of Pathology, University of Utah , Salt Lake City, UT 84112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cory","family":"Teuscher","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Vermont , Burlington, VT 05405"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janis J","family":"Weis","sequence":"additional","affiliation":[{"name":"Division of Microbiology and Immunology, Department of Pathology, University of Utah , Salt Lake City, UT 84112"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2014,12,15]]},"reference":[{"key":"2025030707514225700_r1","doi-asserted-by":"crossref","first-page":"725","DOI":"10.7326\/0003-4819-107-5-725","article-title":"The clinical evolution of Lyme arthritis","volume":"107","author":"Steere","year":"1987","journal-title":"Ann. 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