{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T10:48:46Z","timestamp":1770720526538,"version":"3.49.0"},"reference-count":22,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2005,12,1]],"date-time":"2005-12-01T00:00:00Z","timestamp":1133395200000},"content-version":"vor","delay-in-days":5844,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1989,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>In responder mouse strains repeated injections of subtoxic doses of HgCl<jats:sub>2<\/jats:sub> induce formation of antinuclear autoantibodies (ANA) and antinucleolar autoantibodies (ANolA). Others have shown that responsiveness to HgCl<jats:sub>2<\/jats:sub>\u2010induced formation of ANA and ANolA is linked to H\u20102. Here, we extend these studies to a variety of mouse strains not tested previously. After confirming that strain B10.S (H\u20102<jats:sup>s<\/jats:sup>) is a high responder we have shown that strains B10.D2 (H\u20102<jats:sup>d<\/jats:sup>) and B10.BR (H\u20102<jats:sup>k<\/jats:sup>) are nonresponders. By comparing a panel of strains carrying appropriate intra\u2010H\u20102 recombinant haplotypes derived from <jats:italic>d, k<\/jats:italic> and <jats:italic>s<\/jats:italic>, we were able to map responsiveness to A<jats:sup>s<\/jats:sup>. Interestingly, among four strains all of which were A<jats:sup>s<\/jats:sup>, and thus responsive, only the two H\u20102E<jats:sup>\u2010<\/jats:sup> ones, B10.S and B10.RSD2, were high responders whereas the two H\u20102E<jats:sup>+<\/jats:sup> ones, B10.HTT and B10.S(9R), were significantly less responsive. Thus, the genetics of HgCl<jats:sub>2<\/jats:sub>\u2010induced autoantibody formation follow the rules established for immune responses to a variety of different antigens in that expression of H\u20102E \u201csuppressed\u201d the response.<\/jats:p>","DOI":"10.1002\/eji.1830191212","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T08:04:31Z","timestamp":1172736271000},"page":"2257-2261","source":"Crossref","is-referenced-by-count":72,"title":["Immunological alterations inducible by mercury compounds. III. H\u20102A acts as an immune response and H\u20102E as an immune \u201csuppression\u201d locus for HgCl<sub>2<\/sub>\u2010induced antinucleolar autoantibodies"],"prefix":"10.1002","volume":"19","author":[{"given":"Jasmina","family":"Mirtcheva","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christiane","family":"Pfeiffer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jan Anthonie De","family":"Bruijn","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fr\u00c9D\u00c9Ric","family":"Jacquesmart","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ernst","family":"Gleichmann","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,12]]},"reference":[{"key":"e_1_2_1_2_2","first-page":"347","volume-title":"Autoimmunity and Toxicology","author":"Druet P.","year":"1989"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(86)90046-3"},{"key":"e_1_2_1_4_2","first-page":"269","volume":"71","author":"Hultman P.","year":"1988","journal-title":"Clin. 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