Genetic regulation of anti-erythrocyte autoantibodies and splenomegaly in autoimmune hemolytic anemia-prone New Zealand Black mice
New Zealand Black (NZB) mice spontaneously produce anti-erythrocyte autoantibodies (AEA) in association with splenomegaly, thus serving as a model for autoimmune hemolytic anemia. Although these autoimmune traits are inherited as a dominant fashion, expression in F1 hybrids of NZB and most non-New Z...
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| Veröffentlicht in: | International immunology 2000-01, Vol.12 (1), p.1-8 |
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| creator | Ochiai, Kimiko Ozaki, Shoichi Tanino, Akihiro Watanabe, Shinji Ueno, Tomoo Mitsui, Kenichi Toei, Junichi Inada, Yuji Hirose, Sachiko Shirai, Toshikazu Nishimura, Hiroyuki |
| description | New Zealand Black (NZB) mice spontaneously produce anti-erythrocyte autoantibodies (AEA) in association with splenomegaly, thus serving as a model for autoimmune hemolytic anemia. Although these autoimmune traits are inherited as a dominant fashion, expression in F1 hybrids of NZB and most non-New Zealand strains is suppressed due to the contribution of wild-type modifying genes present in the latter strains. Using chromosomal microsatellite markers in the (C57BL/6 × NZB)F1 × NZB backcross progeny, we mapped C57BL/6 modifying loci for AEA production and splenomegaly. Generation of AEA was found to be down-regulated by a combined effect of two major independently segregating dominant alleles—one linked to D7MIT30 on chromosome 7 and the other linked to D10MIT42 on chromosome 10. Splenomegaly was modified mainly by a single C57BL/6 allele linked to D4MIT58 on chromosome 4. Thus, the autoimmune hemolytic anemia in the NZB strain is under multigenic control and a combined action of not only susceptibility but also modifying alleles with suppressive activities affects the outcome of disease features in the progeny. There are potentially important candidate genes which may be linked to the regulation of AEA and splenomegaly. |
| doi_str_mv | 10.1093/intimm/12.1.1 |
| format | Article |
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Although these autoimmune traits are inherited as a dominant fashion, expression in F1 hybrids of NZB and most non-New Zealand strains is suppressed due to the contribution of wild-type modifying genes present in the latter strains. Using chromosomal microsatellite markers in the (C57BL/6 × NZB)F1 × NZB backcross progeny, we mapped C57BL/6 modifying loci for AEA production and splenomegaly. Generation of AEA was found to be down-regulated by a combined effect of two major independently segregating dominant alleles—one linked to D7MIT30 on chromosome 7 and the other linked to D10MIT42 on chromosome 10. Splenomegaly was modified mainly by a single C57BL/6 allele linked to D4MIT58 on chromosome 4. Thus, the autoimmune hemolytic anemia in the NZB strain is under multigenic control and a combined action of not only susceptibility but also modifying alleles with suppressive activities affects the outcome of disease features in the progeny. There are potentially important candidate genes which may be linked to the regulation of AEA and splenomegaly.</description><identifier>ISSN: 0953-8178</identifier><identifier>EISSN: 1460-2377</identifier><identifier>DOI: 10.1093/intimm/12.1.1</identifier><identifier>PMID: 10607744</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>AEA anti-erythrocyte autoantibody ; Aem anti-erythrocyte autoantibody modifier ; Anemia, Hemolytic, Autoimmune - genetics ; Animals ; anti-erythrocyte autoantibody ; Autoantibodies - genetics ; Autoimmunity - genetics ; Chromosome Mapping ; Crosses, Genetic ; Disease Models, Animal ; Erythrocytes - immunology ; Genetic Predisposition to Disease ; Genotype ; hemolytic anemia ; Lod Score ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NZB - genetics ; microsatellite ; Microsatellite Repeats ; New Zealand Black mice ; QTL quantitative trait locus ; quantitative trait locus ; Quantitative Trait, Heritable ; splenomegaly ; Splenomegaly - genetics ; Spm splenomegaly modifier</subject><ispartof>International immunology, 2000-01, Vol.12 (1), p.1-8</ispartof><rights>Copyright Oxford University Press Jan 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-418c2705d8ee1466ab0dd5721b643a9a1e52a2cc37b5f18120b1086f215a33e63</citedby><cites>FETCH-LOGICAL-c451t-418c2705d8ee1466ab0dd5721b643a9a1e52a2cc37b5f18120b1086f215a33e63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10607744$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ochiai, Kimiko</creatorcontrib><creatorcontrib>Ozaki, Shoichi</creatorcontrib><creatorcontrib>Tanino, Akihiro</creatorcontrib><creatorcontrib>Watanabe, Shinji</creatorcontrib><creatorcontrib>Ueno, Tomoo</creatorcontrib><creatorcontrib>Mitsui, Kenichi</creatorcontrib><creatorcontrib>Toei, Junichi</creatorcontrib><creatorcontrib>Inada, Yuji</creatorcontrib><creatorcontrib>Hirose, Sachiko</creatorcontrib><creatorcontrib>Shirai, Toshikazu</creatorcontrib><creatorcontrib>Nishimura, Hiroyuki</creatorcontrib><title>Genetic regulation of anti-erythrocyte autoantibodies and splenomegaly in autoimmune hemolytic anemia-prone New Zealand Black mice</title><title>International immunology</title><addtitle>Int. Immunol</addtitle><description>New Zealand Black (NZB) mice spontaneously produce anti-erythrocyte autoantibodies (AEA) in association with splenomegaly, thus serving as a model for autoimmune hemolytic anemia. Although these autoimmune traits are inherited as a dominant fashion, expression in F1 hybrids of NZB and most non-New Zealand strains is suppressed due to the contribution of wild-type modifying genes present in the latter strains. Using chromosomal microsatellite markers in the (C57BL/6 × NZB)F1 × NZB backcross progeny, we mapped C57BL/6 modifying loci for AEA production and splenomegaly. Generation of AEA was found to be down-regulated by a combined effect of two major independently segregating dominant alleles—one linked to D7MIT30 on chromosome 7 and the other linked to D10MIT42 on chromosome 10. Splenomegaly was modified mainly by a single C57BL/6 allele linked to D4MIT58 on chromosome 4. Thus, the autoimmune hemolytic anemia in the NZB strain is under multigenic control and a combined action of not only susceptibility but also modifying alleles with suppressive activities affects the outcome of disease features in the progeny. There are potentially important candidate genes which may be linked to the regulation of AEA and splenomegaly.</description><subject>AEA anti-erythrocyte autoantibody</subject><subject>Aem anti-erythrocyte autoantibody modifier</subject><subject>Anemia, Hemolytic, Autoimmune - genetics</subject><subject>Animals</subject><subject>anti-erythrocyte autoantibody</subject><subject>Autoantibodies - genetics</subject><subject>Autoimmunity - genetics</subject><subject>Chromosome Mapping</subject><subject>Crosses, Genetic</subject><subject>Disease Models, Animal</subject><subject>Erythrocytes - immunology</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>hemolytic anemia</subject><subject>Lod Score</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred NZB - genetics</subject><subject>microsatellite</subject><subject>Microsatellite Repeats</subject><subject>New Zealand Black mice</subject><subject>QTL quantitative trait locus</subject><subject>quantitative trait locus</subject><subject>Quantitative Trait, Heritable</subject><subject>splenomegaly</subject><subject>Splenomegaly - genetics</subject><subject>Spm splenomegaly modifier</subject><issn>0953-8178</issn><issn>1460-2377</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFv1DAQRi0EotvCkSuKOHDLdsaO4-RIK2iRViAhqKpeLMeZtG6TeGsnornyy_GyFSAunCzNPD99o4-xVwhrhFocu3Fyw3CMfI1rfMJWWJSQc6HUU7aCWoq8QlUdsMMYbwFA8Fo8ZwcIJShVFCv244xGmpzNAl3PvZmcHzPfZSZZcwrLdBO8XSbKzDz53bDxraOY9m0Wtz2NfqBr0y-ZG38hKco8UnZDg--XndaMNDiTb4NP40_0Pbsi0-9-n_TG3mWDs_SCPetMH-nl43vEvn14__X0PN98Pvt4-m6T20LilBdYWa5AthVROrI0DbStVBybshCmNkiSG26tUI3ssEIODUJVdhylEYJKccTe7r0pzP1McdKDi5b6FIf8HLUCVVcgqv-CqIpSAsgEvvkHvPVzGNMRGmsJQkFdJyjfQzb4GAN1ehvcYMKiEfSuQr2vUCPXqDHxrx-lczNQ-xe97-yP0MWJHn7vTbjTpRJK6vPLK30iNxcXxeUXzcVPtqipKw</recordid><startdate>200001</startdate><enddate>200001</enddate><creator>Ochiai, Kimiko</creator><creator>Ozaki, Shoichi</creator><creator>Tanino, Akihiro</creator><creator>Watanabe, Shinji</creator><creator>Ueno, Tomoo</creator><creator>Mitsui, Kenichi</creator><creator>Toei, Junichi</creator><creator>Inada, Yuji</creator><creator>Hirose, Sachiko</creator><creator>Shirai, Toshikazu</creator><creator>Nishimura, Hiroyuki</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>200001</creationdate><title>Genetic regulation of anti-erythrocyte autoantibodies and splenomegaly in autoimmune hemolytic anemia-prone New Zealand Black mice</title><author>Ochiai, Kimiko ; Ozaki, Shoichi ; Tanino, Akihiro ; Watanabe, Shinji ; Ueno, Tomoo ; Mitsui, Kenichi ; Toei, Junichi ; Inada, Yuji ; Hirose, Sachiko ; Shirai, Toshikazu ; Nishimura, Hiroyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-418c2705d8ee1466ab0dd5721b643a9a1e52a2cc37b5f18120b1086f215a33e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>AEA anti-erythrocyte autoantibody</topic><topic>Aem anti-erythrocyte autoantibody modifier</topic><topic>Anemia, Hemolytic, Autoimmune - genetics</topic><topic>Animals</topic><topic>anti-erythrocyte autoantibody</topic><topic>Autoantibodies - genetics</topic><topic>Autoimmunity - genetics</topic><topic>Chromosome Mapping</topic><topic>Crosses, Genetic</topic><topic>Disease Models, Animal</topic><topic>Erythrocytes - immunology</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>hemolytic anemia</topic><topic>Lod Score</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred NZB - genetics</topic><topic>microsatellite</topic><topic>Microsatellite Repeats</topic><topic>New Zealand Black mice</topic><topic>QTL quantitative trait locus</topic><topic>quantitative trait locus</topic><topic>Quantitative Trait, Heritable</topic><topic>splenomegaly</topic><topic>Splenomegaly - genetics</topic><topic>Spm splenomegaly modifier</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ochiai, Kimiko</creatorcontrib><creatorcontrib>Ozaki, Shoichi</creatorcontrib><creatorcontrib>Tanino, Akihiro</creatorcontrib><creatorcontrib>Watanabe, Shinji</creatorcontrib><creatorcontrib>Ueno, Tomoo</creatorcontrib><creatorcontrib>Mitsui, Kenichi</creatorcontrib><creatorcontrib>Toei, Junichi</creatorcontrib><creatorcontrib>Inada, Yuji</creatorcontrib><creatorcontrib>Hirose, Sachiko</creatorcontrib><creatorcontrib>Shirai, Toshikazu</creatorcontrib><creatorcontrib>Nishimura, Hiroyuki</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ochiai, Kimiko</au><au>Ozaki, Shoichi</au><au>Tanino, Akihiro</au><au>Watanabe, Shinji</au><au>Ueno, Tomoo</au><au>Mitsui, Kenichi</au><au>Toei, Junichi</au><au>Inada, Yuji</au><au>Hirose, Sachiko</au><au>Shirai, Toshikazu</au><au>Nishimura, Hiroyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic regulation of anti-erythrocyte autoantibodies and splenomegaly in autoimmune hemolytic anemia-prone New Zealand Black mice</atitle><jtitle>International immunology</jtitle><addtitle>Int. Immunol</addtitle><date>2000-01</date><risdate>2000</risdate><volume>12</volume><issue>1</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>0953-8178</issn><eissn>1460-2377</eissn><abstract>New Zealand Black (NZB) mice spontaneously produce anti-erythrocyte autoantibodies (AEA) in association with splenomegaly, thus serving as a model for autoimmune hemolytic anemia. Although these autoimmune traits are inherited as a dominant fashion, expression in F1 hybrids of NZB and most non-New Zealand strains is suppressed due to the contribution of wild-type modifying genes present in the latter strains. Using chromosomal microsatellite markers in the (C57BL/6 × NZB)F1 × NZB backcross progeny, we mapped C57BL/6 modifying loci for AEA production and splenomegaly. Generation of AEA was found to be down-regulated by a combined effect of two major independently segregating dominant alleles—one linked to D7MIT30 on chromosome 7 and the other linked to D10MIT42 on chromosome 10. Splenomegaly was modified mainly by a single C57BL/6 allele linked to D4MIT58 on chromosome 4. Thus, the autoimmune hemolytic anemia in the NZB strain is under multigenic control and a combined action of not only susceptibility but also modifying alleles with suppressive activities affects the outcome of disease features in the progeny. There are potentially important candidate genes which may be linked to the regulation of AEA and splenomegaly.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>10607744</pmid><doi>10.1093/intimm/12.1.1</doi><tpages>8</tpages></addata></record> |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | AEA anti-erythrocyte autoantibody Aem anti-erythrocyte autoantibody modifier Anemia, Hemolytic, Autoimmune - genetics Animals anti-erythrocyte autoantibody Autoantibodies - genetics Autoimmunity - genetics Chromosome Mapping Crosses, Genetic Disease Models, Animal Erythrocytes - immunology Genetic Predisposition to Disease Genotype hemolytic anemia Lod Score Mice Mice, Inbred C57BL Mice, Inbred NZB - genetics microsatellite Microsatellite Repeats New Zealand Black mice QTL quantitative trait locus quantitative trait locus Quantitative Trait, Heritable splenomegaly Splenomegaly - genetics Spm splenomegaly modifier |
| title | Genetic regulation of anti-erythrocyte autoantibodies and splenomegaly in autoimmune hemolytic anemia-prone New Zealand Black mice |
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