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- Publisher Website: 10.1084/jem.183.1.329
- Scopus: eid_2-s2.0-0030070349
- PMID: 8551241
- WOS: WOS:A1996TP36500038
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Article: Immunoglobulin-mediated signal transduction in B cells from CD45-deficient mice
Title | Immunoglobulin-mediated signal transduction in B cells from CD45-deficient mice |
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Authors | |
Issue Date | 1996 |
Citation | Journal of Experimental Medicine, 1996, v. 183, n. 1, p. 329-334 How to Cite? |
Abstract | CD45 expression is essential for immunoglobulin (Ig)-mediated B cell activation. Treatments with either anti-Ig or anti-CD45 suggest that CD45 may facilitate early signaling events such as calcium mobilization, and phosphoinositide hydrolysis as well as later events leading to transcription of genes such as c-myc. To examine the role of CD45 more extensively, CD45- deficient mice were generated by disruption of exon 6. Although normal numbers of B cells were found in peripheral lymphoid tissues, CD45-deficient cells failed to proliferate upon IgM cross-linking. In the present study, we demonstrate that the fraction of high buoyant density B cells is reduced while low buoyant density cells are increased. Moreover, there is a significant decline in the number of splenic B cells of the mature IgD(hi), IgM(lo) phenotype. Although both the basal and anti-Ig-induced levels of phosphorylation of Ig-α and phospholipase Cγ2 are indistinguishable from that observed in CD45+ control B cells, a major distinction was found in Ca2+ mobilization. While anti-Ig-induced mobilization of intracellular Ca2+ stores was normal, influx from extracellular sources was abrogated. This finding reveals a novel pathway of regulating B cell responses mediated by CD45. |
Persistent Identifier | http://hdl.handle.net/10722/292509 |
ISSN | 2022 Impact Factor: 15.3 2020 SCImago Journal Rankings: 8.483 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Benatar, Tania | - |
dc.contributor.author | Carsetti, Rita | - |
dc.contributor.author | Furlonger, Caren | - |
dc.contributor.author | Kamalia, Nilupa | - |
dc.contributor.author | Mak, Tak | - |
dc.contributor.author | Paige, Christopher J. | - |
dc.date.accessioned | 2020-11-17T14:56:38Z | - |
dc.date.available | 2020-11-17T14:56:38Z | - |
dc.date.issued | 1996 | - |
dc.identifier.citation | Journal of Experimental Medicine, 1996, v. 183, n. 1, p. 329-334 | - |
dc.identifier.issn | 0022-1007 | - |
dc.identifier.uri | http://hdl.handle.net/10722/292509 | - |
dc.description.abstract | CD45 expression is essential for immunoglobulin (Ig)-mediated B cell activation. Treatments with either anti-Ig or anti-CD45 suggest that CD45 may facilitate early signaling events such as calcium mobilization, and phosphoinositide hydrolysis as well as later events leading to transcription of genes such as c-myc. To examine the role of CD45 more extensively, CD45- deficient mice were generated by disruption of exon 6. Although normal numbers of B cells were found in peripheral lymphoid tissues, CD45-deficient cells failed to proliferate upon IgM cross-linking. In the present study, we demonstrate that the fraction of high buoyant density B cells is reduced while low buoyant density cells are increased. Moreover, there is a significant decline in the number of splenic B cells of the mature IgD(hi), IgM(lo) phenotype. Although both the basal and anti-Ig-induced levels of phosphorylation of Ig-α and phospholipase Cγ2 are indistinguishable from that observed in CD45+ control B cells, a major distinction was found in Ca2+ mobilization. While anti-Ig-induced mobilization of intracellular Ca2+ stores was normal, influx from extracellular sources was abrogated. This finding reveals a novel pathway of regulating B cell responses mediated by CD45. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Experimental Medicine | - |
dc.title | Immunoglobulin-mediated signal transduction in B cells from CD45-deficient mice | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1084/jem.183.1.329 | - |
dc.identifier.pmid | 8551241 | - |
dc.identifier.pmcid | PMC2192424 | - |
dc.identifier.scopus | eid_2-s2.0-0030070349 | - |
dc.identifier.volume | 183 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | 329 | - |
dc.identifier.epage | 334 | - |
dc.identifier.isi | WOS:A1996TP36500038 | - |
dc.identifier.issnl | 0022-1007 | - |