Please use this identifier to cite or link to this item:
https://scholarbank.nus.edu.sg/handle/10635/111797
DC Field | Value | |
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dc.title | B cell development and activation defects resulting in xid-like immunodeficiency in BLNK/SLP-65-deficient mice | |
dc.contributor.author | Xu, S. | |
dc.contributor.author | Tan, J.E.-L. | |
dc.contributor.author | Wong, E.P.-Y. | |
dc.contributor.author | Manickam, A. | |
dc.contributor.author | Ponniah, S. | |
dc.contributor.author | Lam, K.-P. | |
dc.date.accessioned | 2014-11-28T02:49:48Z | |
dc.date.available | 2014-11-28T02:49:48Z | |
dc.date.issued | 2000 | |
dc.identifier.citation | Xu, S.,Tan, J.E.-L.,Wong, E.P.-Y.,Manickam, A.,Ponniah, S.,Lam, K.-P. (2000). B cell development and activation defects resulting in xid-like immunodeficiency in BLNK/SLP-65-deficient mice. International Immunology 12 (3) : 397-404. ScholarBank@NUS Repository. | |
dc.identifier.issn | 09538178 | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/111797 | |
dc.description.abstract | Engagement of the a cell receptor (BCR) leads to the activation of tyrosine kinases and other signaling molecules that ultimately determine the type and magnitude of the B lymphocyte's cellular response. The adaptor protein BLNK/SLP-65 plays a pivotal role in BCR signal transduction by coupling Syk activation to downstream elements such as GrbS, phospholipase C-γ, Vav and Nck. We have generated BLNK(-/-) mice to determine the physiological role of this protein in B cell development and activation. BLNK(-/-) mice exhibit an incomplete block in a cell development with a severe inhibition of pro-B to pre-B cell differentiation. BLNK(-/-) slgM+ cells can develop, seed the peripheral lymphoid tissues and accumulate in numbers overtime. However, these mutant a cells failed to mature and are non-responsive to BCR cross-linking in terms of proliferation and upregulation of activation markers such as CD69 and CD86 (B7-2). In addition, the CD5+ subset of a cells is absent. The immune response to T cell-independent antigen but not T cell-dependent antigen is also impaired. Overall, the phenotype of BLNK(-/-) mice bears a striking resemblance to that of xid mice which is the murine model of human XLA that has a mutation in Bruton's tyrosine kinase. This raises the interesting possibility that mutation in BLNK/SLP-65 may be responsible for certain human immunodeficiencies. | |
dc.source | Scopus | |
dc.subject | Adaptor protein | |
dc.subject | B cell antigen receptor | |
dc.subject | CD5+ B cells | |
dc.subject | Gene targeting | |
dc.subject | Signal transduction | |
dc.type | Article | |
dc.contributor.department | INSTITUTE OF MOLECULAR & CELL BIOLOGY | |
dc.description.sourcetitle | International Immunology | |
dc.description.volume | 12 | |
dc.description.issue | 3 | |
dc.description.page | 397-404 | |
dc.description.coden | INIME | |
dc.identifier.isiut | NOT_IN_WOS | |
Appears in Collections: | Staff Publications |
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