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dc.contributor.authorKlaus, Stephen J.
dc.contributor.authorPhillips, Nancy E.
dc.contributor.authorParker, David C.
dc.date2022-08-11T08:08:59.000
dc.date.accessioned2022-08-23T16:14:51Z
dc.date.available2022-08-23T16:14:51Z
dc.date.issued1993-11-01
dc.date.submitted2008-10-15
dc.identifier.citation<p>Mol Immunol. 1993 Nov;30(16):1553-8.</p>
dc.identifier.issn0161-5890 (Print)
dc.identifier.doi10.1016/0161-5890(93)90463-L
dc.identifier.pmid8232340
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33959
dc.description.abstractEgr-1 is an immediate early gene that is rapidly upregulated in response to mitogenic signals induced by antigen receptor crosslinking on murine B lymphocytes. It has been shown that levels of Egr-1 expression are closely correlated with B cell proliferation in several models of B cell activation and tolerance. We compared the expression of Egr-1 during B cell stimulation with Fab'2 and IgG anti-immunoglobulin (anti-Ig), since it is known that Fab'2 anti-Ig is mitogenic while IgG anti-Ig is not, owing to a dominant inhibitory effect of crosslinking the B cell Fc gamma RII to membrane Ig. While mitogenic doses of Fab'2 anti-Ig induce large and rapid increases in Egr-1 expression, IgG anti-Ig results in smaller increases in Egr-1 mRNA, comparable to that seen with submitogenic concentrations of Fab'2 anti-Ig. However, the correlation between Egr-1 expression and B cell proliferation breaks down when IL-4 is added as a co-mitogen to induce B cell proliferation with IgG anti-Ig or submitogenic concentrations of Fab'2 anti-Ig. No corresponding increases in Egr-1 mRNA levels are observed when IL-4 is added. Therefore, IL-4 overcomes Fc receptor-mediated inhibition of B cell proliferation without affecting inhibition of Egr-1 mRNA induction, as demonstrated earlier for c-myc mRNA in this system.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8232340&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/0161-5890(93)90463-L
dc.subjectAntibodies, Anti-Idiotypic; *Antigens, CD; B-Lymphocytes; Cell Division; Cells, Cultured; DNA-Binding Proteins; Early Growth Response Protein 1; Gene Expression; Humans; Immediate-Early Proteins; Immunoglobulin Fab Fragments; Immunoglobulin G; Interleukin-4; RNA, Messenger; Receptors, IgG; Transcription Factors
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleEffects of IL-4 and Fc gamma receptor II engagement on Egr-1 expression during stimulation of B lymphocytes by membrane immunoglobulin crosslinking
dc.typeJournal Article
dc.source.journaltitleMolecular immunology
dc.source.volume30
dc.source.issue16
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/612
dc.identifier.contextkey651082
html.description.abstract<p>Egr-1 is an immediate early gene that is rapidly upregulated in response to mitogenic signals induced by antigen receptor crosslinking on murine B lymphocytes. It has been shown that levels of Egr-1 expression are closely correlated with B cell proliferation in several models of B cell activation and tolerance. We compared the expression of Egr-1 during B cell stimulation with Fab'2 and IgG anti-immunoglobulin (anti-Ig), since it is known that Fab'2 anti-Ig is mitogenic while IgG anti-Ig is not, owing to a dominant inhibitory effect of crosslinking the B cell Fc gamma RII to membrane Ig. While mitogenic doses of Fab'2 anti-Ig induce large and rapid increases in Egr-1 expression, IgG anti-Ig results in smaller increases in Egr-1 mRNA, comparable to that seen with submitogenic concentrations of Fab'2 anti-Ig. However, the correlation between Egr-1 expression and B cell proliferation breaks down when IL-4 is added as a co-mitogen to induce B cell proliferation with IgG anti-Ig or submitogenic concentrations of Fab'2 anti-Ig. No corresponding increases in Egr-1 mRNA levels are observed when IL-4 is added. Therefore, IL-4 overcomes Fc receptor-mediated inhibition of B cell proliferation without affecting inhibition of Egr-1 mRNA induction, as demonstrated earlier for c-myc mRNA in this system.</p>
dc.identifier.submissionpathgsbs_sp/612
dc.contributor.departmentDepartment of Medicine, Division of Diabetes
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages1553-8


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