pubmed-article:11015437 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11015437 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:11015437 | lifeskim:mentions | umls-concept:C0767393 | lld:lifeskim |
pubmed-article:11015437 | lifeskim:mentions | umls-concept:C1155229 | lld:lifeskim |
pubmed-article:11015437 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
pubmed-article:11015437 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:11015437 | lifeskim:mentions | umls-concept:C1627358 | lld:lifeskim |
pubmed-article:11015437 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:11015437 | pubmed:dateCreated | 2000-11-8 | lld:pubmed |
pubmed-article:11015437 | pubmed:abstractText | B lymphocyte stimulator (BLyS) is a newly identified monocyte-specific TNF family cytokine. It has been implicated in the development of autoimmunity, and functions as a potent costimulator with antiimmunoglobulin M in B cell proliferation in vitro. Here we demonstrate that BLyS prominently enhances the humoral responses to both T cell-independent and T cell-dependent antigens, primarily by attenuation of apoptosis as evidenced by the prolonged survival of antigen-activated B cells in vivo and in vitro. BLyS acts on primary splenic B cells autonomously, and directly cooperates with CD40 ligand (CD40L) in B cell activation in vitro by protecting replicating B cells from apoptosis. Moreover, although BLyS alone cannot activate the cell cycle, it is sufficient to prolong the survival of naive resting B cells in vitro. Attenuation of apoptosis by BLyS correlates with changes in the ratios between Bcl-2 family proteins in favor of cell survival, predominantly by reducing the proapoptotic Bak and increasing its prosurvival partners, Bcl-2 and Bcl-xL. In either resting or CD40L-activated B cells, the NF-kappaB transcription factors RelB and p50 are specifically activated, suggesting that they may mediate BLyS signals for B cell survival. Together, these results provide direct evidence for BLyS enhancement of both T cell-independent and T cell-dependent humoral immune responses, and imply a role for BLyS in the conservation of the B cell repertoire. The ability of BLyS to increase B cell survival indiscriminately, at either a resting or activated state, and to cooperate with CD40L, further suggests that attenuation of apoptosis underlies BLyS enhancement of polyclonal autoimmunity as well as the physiologic humoral immune response. | lld:pubmed |
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pubmed-article:11015437 | pubmed:language | eng | lld:pubmed |
pubmed-article:11015437 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11015437 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11015437 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11015437 | pubmed:month | Oct | lld:pubmed |
pubmed-article:11015437 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:11015437 | pubmed:author | pubmed-author:LeeHH | lld:pubmed |
pubmed-article:11015437 | pubmed:author | pubmed-author:Chen-KiangSS | lld:pubmed |
pubmed-article:11015437 | pubmed:author | pubmed-author:HatadaEE | lld:pubmed |
pubmed-article:11015437 | pubmed:author | pubmed-author:XuQ ZQZ | lld:pubmed |
pubmed-article:11015437 | pubmed:author | pubmed-author:HilbertDD | lld:pubmed |
pubmed-article:11015437 | pubmed:author | pubmed-author:TourignyM RMR | lld:pubmed |
pubmed-article:11015437 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11015437 | pubmed:day | 2 | lld:pubmed |
pubmed-article:11015437 | pubmed:volume | 192 | lld:pubmed |
pubmed-article:11015437 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11015437 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11015437 | pubmed:pagination | 953-64 | lld:pubmed |
pubmed-article:11015437 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
pubmed-article:11015437 | pubmed:meshHeading | pubmed-meshheading:11015437... | lld:pubmed |
pubmed-article:11015437 | pubmed:meshHeading | pubmed-meshheading:11015437... | lld:pubmed |
pubmed-article:11015437 | pubmed:meshHeading | pubmed-meshheading:11015437... | lld:pubmed |