Current Perspectives on Primary Immunodeficiency Diseases
Identifieur interne : 003C91 ( Pmc/Checkpoint ); précédent : 003C90; suivant : 003C92Current Perspectives on Primary Immunodeficiency Diseases
Auteurs : Arvind Kumar ; Suzanne S. Teuber ; M. Eric GershwinSource :
- Clinical and Developmental Immunology [ 1740-2522 ] ; 2006.
Abstract
Since the original description of X-linked agammaglobulinemia in 1952, the number of independent primary immunodeficiency diseases (PIDs) has expanded to more than 100 entities. By definition, a PID is a genetically determined disorder resulting in enhanced susceptibility to infectious disease. Despite the heritable nature of these diseases, some PIDs are clinically manifested only after prerequisite environmental exposures but they often have associated malignant, allergic, or autoimmune manifestations. PIDs must be distinguished from secondary or acquired immunodeficiencies, which are far more common. In this review, we will place these immunodeficiencies in the context of both clinical and laboratory presentations as well as highlight the known genetic basis.
Url:
DOI: 10.1080/17402520600800705
PubMed: 17162365
PubMed Central: 2270780
Affiliations:
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Clin Dev Immunol</journal-id><journal-title>Clinical and Developmental Immunology</journal-title><issn pub-type="ppub">1740-2522</issn><issn pub-type="epub">1740-2530</issn><publisher><publisher-name>Hindawi Publishing Corporation</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">17162365</article-id><article-id pub-id-type="pmc">2270780</article-id><article-id pub-id-type="pii">S1740252206000229</article-id><article-id pub-id-type="doi">10.1080/17402520600800705</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Current Perspectives on Primary Immunodeficiency Diseases</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Kumar</surname><given-names>Arvind</given-names></name></contrib><contrib contrib-type="author"><name><surname>Teuber</surname><given-names>Suzanne S.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Gershwin</surname><given-names>M. Eric</given-names></name></contrib></contrib-group><aff id="aff"><label></label><addr-line>Division of Rheumatology</addr-line><addr-line>Allergy and Clinical Immunology</addr-line><addr-line>Department of Internal Medicine</addr-line><addr-line>University of California at Davis School of Medicine</addr-line><addr-line>Davis</addr-line><addr-line>CA</addr-line><country>USA</country></aff><pub-date pub-type="ppub"><season>Jun-Dec</season><year>2006</year></pub-date><volume>13</volume><issue>2-4</issue><fpage>223</fpage><lpage>259</lpage><permissions><copyright-statement>Copyright © 2006 Hindawi Publishing Corporation.</copyright-statement><copyright-year>2006</copyright-year><copyright-holder>Hindawi Publishing Corporation</copyright-holder><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/"><p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p></license></permissions><abstract><p>Since the original description of X-linked agammaglobulinemia in 1952, the number of independent primary immunodeficiency diseases (PIDs) has expanded to more than 100 entities. By definition, a PID is a genetically determined disorder resulting in enhanced susceptibility to infectious disease. Despite the heritable nature of these diseases, some PIDs are clinically manifested only after prerequisite environmental exposures but they often have associated malignant, allergic, or autoimmune manifestations. PIDs must be distinguished from secondary or acquired immunodeficiencies, which are far more common. In this review, we will place these immunodeficiencies in the context of both clinical and laboratory presentations as well as highlight the known genetic basis.</p></abstract></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Gershwin, M Eric" sort="Gershwin, M Eric" uniqKey="Gershwin M" first="M. Eric" last="Gershwin">M. Eric Gershwin</name><name sortKey="Kumar, Arvind" sort="Kumar, Arvind" uniqKey="Kumar A" first="Arvind" last="Kumar">Arvind Kumar</name><name sortKey="Teuber, Suzanne S" sort="Teuber, Suzanne S" uniqKey="Teuber S" first="Suzanne S." last="Teuber">Suzanne S. Teuber</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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