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The effects of anti-idiotypic antibody on antibody production and apoptosis of anti-dsDNA antibody producing cells

DC Field Value Language
dc.contributor.author이수곤-
dc.date.accessioned2015-07-15T16:54:27Z-
dc.date.available2015-07-15T16:54:27Z-
dc.date.issued2003-
dc.identifier.issn0392-856X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/113836-
dc.description.abstractOBJECTIVE: Systemic lupus erythematosus is an autoimmune disease characterized by the production of anti-dsDNA antibody. Because the titer of anti-dsDNA antibody is correlated with disease severity, especially in lupus nephritis, controlling anti-dsDNA antibody production is important in the treatment of SLE. There are many regulatory mechanisms of autoantibody production; one of these is the interaction between idiotype and anti-idiotype antibody (anti-Id). The purpose of the present study was to assess the effect of anti-Id on anti-dsDNA antibody production and apoptosis and to study the mechanism of anti-Id induced apoptosis. METHODS: After anti-dsDNA antibody producing hybridomas were treated with anti-Id, we checked the amount of anti-dsDNA antibody production, the rate of transcription, cellular proliferation, and apoptosis. Also, after treatment with anti-oxidant (N-acetyl-Lcysteine), phorbol esters with calcium ionophore and corticosteroids, we compared their effect on apoptosis with anti-Id. RESULTS: Two types of anti-dsDNA antibody producing hybridomas (G1-2, gamma and kappa chains; M2-10, mu and kappa chains) were treated with anti-Id and it was found that: (1) the amount of anti-dsDNA antibody production decreased; (2) the rate of transcription and cellular proliferation did not decrease; and (3) the level of apoptosis increased. The two cells expressed Fas and Fas-ligand, and the Fas of G1-2 was functional but that of M2-10 was not. The treatment of these cells with anti-Id resulted in no change in Fas-ligand and Bax expression, but the expression of Bcl-2 was decreased. In addition, treatment with antioxidant (N-acetyl-L-cysteine) inhibited anti-Id-induced apoptosis in G1-2 and M2-10. Phorbol esters with calcium ionophore also inhibited anti-Id induced apoptosis in M2-10. Corticosteroids induced apoptosis in both cells and showed similar results with anti-Id induced apoptosis. CONCLUSION: The anti-Id suppressed the production of anti-dsDNA antibody in two cells by inducing apoptosis, as did prednisolone. Furthermore, Bcl-2, oxygen-free radicals and protein kinase C might be involved in the induction of apoptosis by anti-Id.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfCLINICAL AND EXPERIMENTAL RHEUMATOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHAntibodies, Anti-Idiotypic/pharmacology*-
dc.subject.MESHAntibodies, Antinuclear/biosynthesis*-
dc.subject.MESHAntibodies, Antinuclear/immunology-
dc.subject.MESHAntibody Formation-
dc.subject.MESHAntibody-Producing Cells/drug effects-
dc.subject.MESHAntibody-Producing Cells/immunology*-
dc.subject.MESHApoptosis/drug effects-
dc.subject.MESHApoptosis/immunology*-
dc.subject.MESHBlotting, Northern-
dc.subject.MESHBlotting, Western-
dc.subject.MESHCells, Cultured-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHElectrophoresis-
dc.subject.MESHEnzyme-Linked Immunosorbent Assay-
dc.subject.MESHFlow Cytometry-
dc.subject.MESHLupus Erythematosus, Systemic/immunology*-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred MRL lpr-
dc.subject.MESHPrednisolone/pharmacology*-
dc.subject.MESHSensitivity and Specificity-
dc.titleThe effects of anti-idiotypic antibody on antibody production and apoptosis of anti-dsDNA antibody producing cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorC.H. Lee-
dc.contributor.googleauthorC.H. Suh-
dc.contributor.googleauthorS.K. Lee-
dc.contributor.googleauthorY.T. Kim-
dc.contributor.googleauthorJ. Lee-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02889-
dc.relation.journalcodeJ00555-
dc.identifier.eissn1593-098X-
dc.identifier.pmid12846046-
dc.identifier.urlhttp://www.clinexprheumatol.org/abstract.asp?a=2054-
dc.subject.keyword12846046-
dc.contributor.alternativeNameLee, Soo Kon-
dc.contributor.affiliatedAuthorLee, Soo Kon-
dc.rights.accessRightsnot free-
dc.citation.volume21-
dc.citation.number3-
dc.citation.startPage291-
dc.citation.endPage300-
dc.identifier.bibliographicCitationCLINICAL AND EXPERIMENTAL RHEUMATOLOGY, Vol.21(3) : 291-300, 2003-
dc.identifier.rimsid41423-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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