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<title xml:lang="en">Genetic segregation analyses of serum IgG2 levels.</title>
<author>
<name sortKey="Marazita, M L" sort="Marazita, M L" uniqKey="Marazita M" first="M. L." last="Marazita">M. L. Marazita</name>
</author>
<author>
<name sortKey="Lu, H" sort="Lu, H" uniqKey="Lu H" first="H." last="Lu">H. Lu</name>
</author>
<author>
<name sortKey="Cooper, M E" sort="Cooper, M E" uniqKey="Cooper M" first="M. E." last="Cooper">M. E. Cooper</name>
</author>
<author>
<name sortKey="Quinn, S M" sort="Quinn, S M" uniqKey="Quinn S" first="S. M." last="Quinn">S. M. Quinn</name>
</author>
<author>
<name sortKey="Zhang, J" sort="Zhang, J" uniqKey="Zhang J" first="J." last="Zhang">J. Zhang</name>
</author>
<author>
<name sortKey="Burmeister, J A" sort="Burmeister, J A" uniqKey="Burmeister J" first="J. A." last="Burmeister">J. A. Burmeister</name>
</author>
<author>
<name sortKey="Califano, J V" sort="Califano, J V" uniqKey="Califano J" first="J. V." last="Califano">J. V. Califano</name>
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<author>
<name sortKey="Pandey, J P" sort="Pandey, J P" uniqKey="Pandey J" first="J. P." last="Pandey">J. P. Pandey</name>
</author>
<author>
<name sortKey="Schenkein, H A" sort="Schenkein, H A" uniqKey="Schenkein H" first="H. A." last="Schenkein">H. A. Schenkein</name>
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<author>
<name sortKey="Tew, J G" sort="Tew, J G" uniqKey="Tew J" first="J. G." last="Tew">J. G. Tew</name>
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<idno type="pmid">8651265</idno>
<idno type="pmc">1914630</idno>
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<idno type="RBID">PMC:1914630</idno>
<date when="1996">1996</date>
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<title xml:lang="en" level="a" type="main">Genetic segregation analyses of serum IgG2 levels.</title>
<author>
<name sortKey="Marazita, M L" sort="Marazita, M L" uniqKey="Marazita M" first="M. L." last="Marazita">M. L. Marazita</name>
</author>
<author>
<name sortKey="Lu, H" sort="Lu, H" uniqKey="Lu H" first="H." last="Lu">H. Lu</name>
</author>
<author>
<name sortKey="Cooper, M E" sort="Cooper, M E" uniqKey="Cooper M" first="M. E." last="Cooper">M. E. Cooper</name>
</author>
<author>
<name sortKey="Quinn, S M" sort="Quinn, S M" uniqKey="Quinn S" first="S. M." last="Quinn">S. M. Quinn</name>
</author>
<author>
<name sortKey="Zhang, J" sort="Zhang, J" uniqKey="Zhang J" first="J." last="Zhang">J. Zhang</name>
</author>
<author>
<name sortKey="Burmeister, J A" sort="Burmeister, J A" uniqKey="Burmeister J" first="J. A." last="Burmeister">J. A. Burmeister</name>
</author>
<author>
<name sortKey="Califano, J V" sort="Califano, J V" uniqKey="Califano J" first="J. V." last="Califano">J. V. Califano</name>
</author>
<author>
<name sortKey="Pandey, J P" sort="Pandey, J P" uniqKey="Pandey J" first="J. P." last="Pandey">J. P. Pandey</name>
</author>
<author>
<name sortKey="Schenkein, H A" sort="Schenkein, H A" uniqKey="Schenkein H" first="H. A." last="Schenkein">H. A. Schenkein</name>
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<name sortKey="Tew, J G" sort="Tew, J G" uniqKey="Tew J" first="J. G." last="Tew">J. G. Tew</name>
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<title level="j">American Journal of Human Genetics</title>
<idno type="ISSN">0002-9297</idno>
<idno type="eISSN">1537-6605</idno>
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<date when="1996">1996</date>
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<div type="abstract" xml:lang="en">
<p>Summary : The aim of this study was to determine whether there was evidence for a genetic component in the immune response as measured by IgG2 levels. The study was motivated by our studies of early-onset periodontitis (EOP), a group of disorders characterized by rapid destruction of the supporting tissues of the teeth in otherwise healthy individuals. EOP has two subforms, localized juvenile periodontitis (LJP) and a generalized form (G-EOP). IgG2 levels are elevated in LJP but not G-EOP individuals; and African-American IgG2 levels are higher than Caucasian levels regardless of EOP status. IgG2 levels were determined in 123 EOP families and in 508 unrelated non-EOP control individuals. Segregation analysis under the regressive model approach of Bonney was used to analyze IgG2 levels for evidence of major locus segregation. After adjusting for LJP status, race, sex, and age, the best fitting model was an autosomal codominant major locus model (accounting for approximately 62% of the variance in IgG2), plus residual parent/offspring and spousal correlations. Smoking and GM23 are also known to affect IgG2 levels. If additional adjustments are made for smoking and GM23, the best-fitting model is still a codominant major locus but with no significant residual correlations.</p>
</div>
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<pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front>
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<journal-id journal-id-type="nlm-ta">Am J Hum Genet</journal-id>
<journal-title>American Journal of Human Genetics</journal-title>
<issn pub-type="ppub">0002-9297</issn>
<issn pub-type="epub">1537-6605</issn>
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<article-meta>
<article-id pub-id-type="pmid">8651265</article-id>
<article-id pub-id-type="pmc">1914630</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Research Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Genetic segregation analyses of serum IgG2 levels.</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Marazita</surname>
<given-names>M. L.</given-names>
</name>
<email>mlm3@vms.cis.pitt.edu</email>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Lu</surname>
<given-names>H.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Cooper</surname>
<given-names>M. E.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Quinn</surname>
<given-names>S. M.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zhang</surname>
<given-names>J.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Burmeister</surname>
<given-names>J. A.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Califano</surname>
<given-names>J. V.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Pandey</surname>
<given-names>J. P.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Schenkein</surname>
<given-names>H. A.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Tew</surname>
<given-names>J. G.</given-names>
</name>
</contrib>
</contrib-group>
<aff>Cleft Palate-Craniofacial Center, Department of Oral and Maxillofacial Surgery, University of Pittsburgh, Pennsylvania 15261, USA.</aff>
<pub-date pub-type="ppub">
<month>5</month>
<year>1996</year>
</pub-date>
<volume>58</volume>
<issue>5</issue>
<fpage>1042</fpage>
<lpage>1049</lpage>
<abstract>
<p>Summary : The aim of this study was to determine whether there was evidence for a genetic component in the immune response as measured by IgG2 levels. The study was motivated by our studies of early-onset periodontitis (EOP), a group of disorders characterized by rapid destruction of the supporting tissues of the teeth in otherwise healthy individuals. EOP has two subforms, localized juvenile periodontitis (LJP) and a generalized form (G-EOP). IgG2 levels are elevated in LJP but not G-EOP individuals; and African-American IgG2 levels are higher than Caucasian levels regardless of EOP status. IgG2 levels were determined in 123 EOP families and in 508 unrelated non-EOP control individuals. Segregation analysis under the regressive model approach of Bonney was used to analyze IgG2 levels for evidence of major locus segregation. After adjusting for LJP status, race, sex, and age, the best fitting model was an autosomal codominant major locus model (accounting for approximately 62% of the variance in IgG2), plus residual parent/offspring and spousal correlations. Smoking and GM23 are also known to affect IgG2 levels. If additional adjustments are made for smoking and GM23, the best-fitting model is still a codominant major locus but with no significant residual correlations.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>

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