2009年8月
The lectin Jacalin induces human B-lymphocyte apoptosis through glycosylation-dependent interaction with CD45
IMMUNOLOGY
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- 巻
- 127
- 号
- 4
- 開始ページ
- 477
- 終了ページ
- 488
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1111/j.1365-2567.2008.02977.x
- 出版者・発行元
- WILEY-BLACKWELL PUBLISHING, INC
P>It has been well established that CD45 is a key receptor-type protein tyrosine phosphatase (PTPase) regulating Src-family protein tyrosine kinase (Src-PTK) in T and B lymphocytes. However, precisely how CD45 exerts its effect in these lymphocytes remains controversial. We recently reported that Jacalin, an alpha-O-glycoside of the disaccharide Thomsen-Friedenreich antigen-specific lectin from jackfruit seeds, caused marked T-cell activation in response to T-cell receptor ligation and CD28 costimulation by binding to CD45. On extending the reported research, we found that CD45 and isoforms are major Jacalin receptors on B lymphocytes, and that the glycosylation of CD45 is involved in the interaction of Jacalin with the PTPase. In contrast to Jacalin-stimulated T-cell activation, we found that Jacalin induced human B-lymphocyte apoptosis, resulting in calcium mobilization and calpain activation, suggesting that the calcium-calpain pathway may mediate the Jacalin-induced apoptosis. Importantly, the apoptosis was effectively blocked by a specific CD45 PTPase inhibitor, indicating that Jacalin induces human B-lymphocyte apoptosis through CD45 triggering. Furthermore, we found that Jacalin significantly increased the C-terminal inhibitory tyrosine (Tyr507) phosphorylation of Src-PTK Lyn, one of the major substrates of CD45 PTPase, and this effect was also observed on incubation of B lymphocytes with the specific CD45 PTPase inhibitor, suggesting that Jacalin stimulation results in increasing C-terminal tyrosine phosphorylation of the kinase through inhibition of CD45 tyrosine phosphatase activity in human B lymphocytes. Therefore, the down-modulation of Lyn kinase may play a role in the regulation of B-lymphocyte viability.
- リンク情報
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- DOI
- https://doi.org/10.1111/j.1365-2567.2008.02977.x
- CiNii Articles
- http://ci.nii.ac.jp/naid/80020477051
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/19175793
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000267752700005&DestApp=WOS_CPL
- ID情報
-
- DOI : 10.1111/j.1365-2567.2008.02977.x
- ISSN : 0019-2805
- CiNii Articles ID : 80020477051
- PubMed ID : 19175793
- Web of Science ID : WOS:000267752700005