File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Production of anti-phosphorylcholine antibodies of the T15 idiotype in CBA/N xid mice: Investigation of the defect using a T15 immunoglobulin transgene

TitleProduction of anti-phosphorylcholine antibodies of the T15 idiotype in CBA/N xid mice: Investigation of the defect using a T15 immunoglobulin transgene
Authors
Issue Date1994
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/molimm
Citation
Molecular Immunology, 1994, v. 31 n. 5, p. 351-359 How to Cite?
AbstractA notable defect in CBA/N xid mice is their relative inability to make antibodies to phosphorylcholine (PC), particularly those of the T15 idiotype which predominate in the anti-PC responses of immunologically normal mice. To investigate the basis of this defect, we introduced functionally rearranged genes encoding a T15 + PC-binding immunoglobulin G antibody into the germline of these animals. Expression of these genes in the xid cells was observed, shown by the existence of a distinct population of T15 + cells (3 x 10 6) in the spleen of the transgenic animals, and the presence of PC-binding T15 + IgG antibodies (1-15 μg/ml) in the serum. Mixed antibody molecules were also found, however, which were composed of both transgene-encoded and endogenously-derived chains. Existence of the T15 + cells in these animals seemed normal, since these were not depleted (to any great extent) and were immunocompetent as well. The latter was shown by the increased T15 + antibody production in the transgenic animals when stimulated with a PC-associated thymus-independent type I (TI-1) antigen and anti-idiotype antibodies, but not with the pneumococcal TI-2 antigen. This is similar to the PC-specific (T15 -) responsiveness of normal CBA/N xid mice. Based on these results, we argue that a reason why T15 + antibodies are not normally made by CBA/N xid animals is because T15 + genes are not utilized or, as with any T15 + precursors present, selected for in these animals, in contrast to normal mice where the Lyb-5 or CD5 cells (which are absent in CBA/N xid animals) are known to be specially endowed to make such antibodies.
Persistent Identifierhttp://hdl.handle.net/10722/178564
ISSN
2015 Impact Factor: 3.375
2015 SCImago Journal Rankings: 1.524
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLim, PLen_US
dc.contributor.authorChan, STHen_US
dc.contributor.authorLeung, DTMen_US
dc.contributor.authorNg, SSMen_US
dc.contributor.authorLoh, TTen_US
dc.date.accessioned2012-12-19T09:48:24Z-
dc.date.available2012-12-19T09:48:24Z-
dc.date.issued1994en_US
dc.identifier.citationMolecular Immunology, 1994, v. 31 n. 5, p. 351-359en_US
dc.identifier.issn0161-5890en_US
dc.identifier.urihttp://hdl.handle.net/10722/178564-
dc.description.abstractA notable defect in CBA/N xid mice is their relative inability to make antibodies to phosphorylcholine (PC), particularly those of the T15 idiotype which predominate in the anti-PC responses of immunologically normal mice. To investigate the basis of this defect, we introduced functionally rearranged genes encoding a T15 + PC-binding immunoglobulin G antibody into the germline of these animals. Expression of these genes in the xid cells was observed, shown by the existence of a distinct population of T15 + cells (3 x 10 6) in the spleen of the transgenic animals, and the presence of PC-binding T15 + IgG antibodies (1-15 μg/ml) in the serum. Mixed antibody molecules were also found, however, which were composed of both transgene-encoded and endogenously-derived chains. Existence of the T15 + cells in these animals seemed normal, since these were not depleted (to any great extent) and were immunocompetent as well. The latter was shown by the increased T15 + antibody production in the transgenic animals when stimulated with a PC-associated thymus-independent type I (TI-1) antigen and anti-idiotype antibodies, but not with the pneumococcal TI-2 antigen. This is similar to the PC-specific (T15 -) responsiveness of normal CBA/N xid mice. Based on these results, we argue that a reason why T15 + antibodies are not normally made by CBA/N xid animals is because T15 + genes are not utilized or, as with any T15 + precursors present, selected for in these animals, in contrast to normal mice where the Lyb-5 or CD5 cells (which are absent in CBA/N xid animals) are known to be specially endowed to make such antibodies.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/molimmen_US
dc.relation.ispartofMolecular Immunologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntibody Formationen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshGenetic Linkageen_US
dc.subject.meshImmunoglobulin Idiotypes - Biosynthesis - Geneticsen_US
dc.subject.meshImmunologic Deficiency Syndromes - Genetics - Immunologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Cbaen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshPhosphorylcholine - Immunologyen_US
dc.subject.meshX Chromosomeen_US
dc.titleProduction of anti-phosphorylcholine antibodies of the T15 idiotype in CBA/N xid mice: Investigation of the defect using a T15 immunoglobulin transgeneen_US
dc.typeArticleen_US
dc.identifier.emailNg, SSM: ssmng@hku.hken_US
dc.identifier.authorityNg, SSM=rp00767en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0161-5890(94)90113-9en_US
dc.identifier.pmid8152438-
dc.identifier.scopuseid_2-s2.0-0028230610en_US
dc.identifier.volume31en_US
dc.identifier.issue5en_US
dc.identifier.spage351en_US
dc.identifier.epage359en_US
dc.identifier.isiWOS:A1994ND63900004-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLim, PL=7202592401en_US
dc.identifier.scopusauthoridChan, STH=55455845100en_US
dc.identifier.scopusauthoridLeung, DTM=7203002802en_US
dc.identifier.scopusauthoridNg, SSM=7403358718en_US
dc.identifier.scopusauthoridLoh, TT=36849142100en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats