{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,11,12]],"date-time":"2023-11-12T09:25:36Z","timestamp":1699781136793},"reference-count":17,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2005,11,16]],"date-time":"2005-11-16T00:00:00Z","timestamp":1132099200000},"content-version":"vor","delay-in-days":10973,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1975,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>H\u20102\u2010linked immune response (Ir) genes specifically and distinctly control immunological responsiveness of mice to the non\u2010cross\u2010reacting enzyme antigens LDH<jats:sub>A<\/jats:sub> and LDH<jats:sub>B<\/jats:sub>. In a previous study (Melchers, I., Rajewsky, K. and Shreffler, D. C., <jats:italic>Eur. J. Immunol.<\/jats:italic> 1973. <jats:italic>3<\/jats:italic>: 754) two levels of responsiveness to LDH<jats:sub>B<\/jats:sub> were found and mice could be classified into high and low responders (HR or LR). We now detect a third, intermediate level of responsiveness. In addition, in certain crosses, \u201csuperhigh\u201d responses as well as responses in between the low and intermediate level are found. An apparently highly polymorphic system of Ir genes thus determines the level of responsiveness in a surprisingly discrete and precise way.<\/jats:p><jats:p>In general, high or intermediate responsiveness was dominant over low responsiveness in F<jats:sub>1<\/jats:sub> animals. In one out of four cases the cross between an intermediate responder (IMR) and a LR, which were congenic for H\u20102, resulted in a level of responsiveness in between that of the two parental strains.<\/jats:p><jats:p>In crosses between IMR strains, the F<jats:sub>1<\/jats:sub> animals were either again IMR or showed functional complementation to high responsiveness in two out of four combinations. The results can be explained in terms of two polymorphic loci which interact in the control of responsiveness to LDH<jats:sub>B<\/jats:sub>.<\/jats:p><jats:p>Surprisingly, the B10.HTT strain, which carries the recombinant H\u20102<jats:sup>t3<\/jats:sup> chromosome, is an IMR, although the H\u20102<jats:sup>t3<\/jats:sup> chromosome carries the HR H\u20102<jats:sup>s<\/jats:sup> allele in the Ir\u20101B region, to which Ir\u2010LDH<jats:sub>B<\/jats:sub> has been previously mapped. Complementation to high responsiveness is achieved when the H\u20102<jats:sup>t3<\/jats:sup> chromosome is combined in an F<jats:sub>1<\/jats:sub> cross with the H\u20102 chromosome from LR strains carrying \u201csilent\u201d HR alleles in the I\u2010C and\/or S regions (H\u20102<jats:sup>a<\/jats:sup> and H\u20102<jats:sup>h2<\/jats:sup>).<\/jats:p><jats:p>This demonstrates that the response to LDH<jats:sub>B<\/jats:sub> is controlled by at least two separate, interacting loci within the H\u20102 complex. One of these loci maps, at least in the case of H\u20102<jats:sup>s<\/jats:sup> and H\u20102<jats:sup>d<\/jats:sup>, to the left of the I\u2010C region, whereas the other is located in I\u2010C or S, as again shown for the H\u20102<jats:sup>d<\/jats:sup> and H\u20102<jats:sup>s<\/jats:sup> haplotypes. One may speculate that these loci also mediate complementation between our IMR strains (see above) and exert distinct functions in the Ir gene control of the immune response.<\/jats:p>","DOI":"10.1002\/eji.1830051105","type":"journal-article","created":{"date-parts":[[2007,2,28]],"date-time":"2007-02-28T01:06:48Z","timestamp":1172624808000},"page":"753-759","source":"Crossref","is-referenced-by-count":38,"title":["Specific control of responsiveness by two complementing Ir loci in the H\u20102 complex"],"prefix":"10.1002","volume":"5","author":[{"given":"Inga","family":"Melchers","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Rajewsky","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,11,16]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2776(08)60208-4"},{"key":"e_1_2_1_3_2","volume":"21","author":"Benacerraf B.","year":"1975","journal-title":"Advan. Cancer Res."},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF01564092"},{"key":"e_1_2_1_5_2","first-page":"53","volume":"53","author":"R\u00fcde E.","year":"1973","journal-title":"Behring Inst. Mitt."},{"key":"e_1_2_1_6_2","doi-asserted-by":"crossref","first-page":"1238","DOI":"10.4049\/jimmunol.110.5.1238","volume":"110","author":"Zaleski M.","year":"1973","journal-title":"J. Immunol."},{"key":"e_1_2_1_7_2","unstructured":"Melchers I. Ph. D. Thesis University of Cologne1975."},{"key":"e_1_2_1_8_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF01564058"},{"key":"e_1_2_1_9_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.126.4.581"},{"key":"e_1_2_1_10_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830031204"},{"key":"e_1_2_1_11_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF01564047"},{"key":"e_1_2_1_12_2","first-page":"1507","volume":"5","author":"Meo T.","year":"1973","journal-title":"Transplant. 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