CD4+ cells treated with DNA methylation inhibitors induce autologous B cell differentiation
dc.contributor.author | Richardson, Bruce C. | en_US |
dc.contributor.author | Liebling, Michael R. | en_US |
dc.contributor.author | Hudson, Jerry L. | en_US |
dc.date.accessioned | 2006-04-10T13:43:13Z | |
dc.date.available | 2006-04-10T13:43:13Z | |
dc.date.issued | 1990-06 | en_US |
dc.identifier.citation | Richardson, Bruce C., Liebling, Michael R., Hudson, Jerry L. (1990/06)."CD4+ cells treated with DNA methylation inhibitors induce autologous B cell differentiation." Clinical Immunology and Immunopathology 55(3): 368-381. <http://hdl.handle.net/2027.42/28550> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6WCK-4BJW42M-1PB/2/956191d73433794e976906bbbfef58aa | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/28550 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1692774&dopt=citation | en_US |
dc.description.abstract | The DNA methylation inhibitor 5-azacytidine induces autoreactivity in cloned CD4+ T cells, but the functional consequences of this response are unknown. We now report that CD4+ T cells treated with 5-azacytidine respond to autologous antigen-presenting cells and induce autologous B cell differentiation without exogenous antigen or mitogen. This mechanism could play a role in some autoimmune diseases characterized by T cell DNA hypomethylation and polyclonal B cell activation. | en_US |
dc.format.extent | 1050394 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | CD4+ cells treated with DNA methylation inhibitors induce autologous B cell differentiation | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Microbiology and Immunology | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | UCLA School of Medicine, Los Angeles, California 90024, USA; University of Michigan, Ann Arbor, Michigan 48109-0531, USA. | en_US |
dc.contributor.affiliationum | UCLA School of Medicine, Los Angeles, California 90024, USA; University of Michigan, Ann Arbor, Michigan 48109-0531, USA. | en_US |
dc.contributor.affiliationum | UCLA School of Medicine, Los Angeles, California 90024, USA; University of Michigan, Ann Arbor, Michigan 48109-0531, USA. | en_US |
dc.identifier.pmid | 1692774 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/28550/1/0000349.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0090-1229(90)90125-A | en_US |
dc.identifier.source | Clinical Immunology and Immunopathology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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