Document Detail


Scarcity of lambda 1 B cells in mice with a single point mutation in C lambda 1 is due to a low BCR signal caused by misfolded lambda 1 light chain.
MedLine Citation:
PMID:  16860389     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The presence of valine-154 instead of glycine in the constant region of lambda1 causes a severe lambda1 B cell defect in SJL and lambda1-valine knock-in mice with a compensatory increase in lambda2,3 B cells. The defect is due to low signaling by the lambda1-valine BCR. lambda1-Valine B cells deficient in the SHP-1 phosphatase survive better than lambda2,3 B cells in these mice, or lambda1 B cells in lambda1 wildtype mice. Low signaling is apparently due to misfolding of the lambda1-valine light chain as demonstrated by the absence of a regular beta-sheet structure determined by circular dichroism, the sedimentation of the light chain in solution, and the association of valine-valine constant regions in a yeast two-hybrid assay. lambda1-Valine B cells that survive apparently have a higher BCR signal, presumably because of their specific lambda1-heavy chain combination or having encountered a high-affiniy antigen. lambda1-Valine mice have increased B1 cells which were shown by others to have a higher signaling potential. Valine mice crossed with non-conventional gamma2b transgenic mice, in which B cell development is accelerated and in which B1 cells and high signaling cells are greatly reduced, have essentially no, lambda2,3 B cells, but increased numbers of lambda1-valine B cells. This supports the conclusion that the major defect in lambda1-valine mice is the inability of valine-preB cells to produce a threshold signal for B cell development. The reduction of lambda2,3 B cells in valine mice with a gamma2b transgene shows that the majority of their compensatory increase is almost entirely of the B1 cell type.
Authors:
Veronica V Volgina; Tianhe Sun; Grazyna Bozek; Terence E Martin; Ursula Storb
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-07-24
Journal Detail:
Title:  Molecular immunology     Volume:  44     ISSN:  0161-5890     ISO Abbreviation:  Mol. Immunol.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2006-09-26     Completed Date:  2007-03-05     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  7905289     Medline TA:  Mol Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1417-28     Citation Subset:  IM    
Affiliation:
Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, IL 60637, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
B-Lymphocyte Subsets / immunology*,  metabolism*
Cells, Cultured
Immunoglobulin Constant Regions / biosynthesis,  genetics*
Immunoglobulin Heavy Chains / biosynthesis,  genetics
Immunoglobulin Light Chains / biosynthesis,  genetics*
Lymphocyte Count
Mice
Mice, Knockout
Mice, Transgenic
Point Mutation / genetics*
Protein Folding*
Receptors, Antigen, B-Cell / chemistry,  genetics,  physiology*
Signal Transduction / genetics,  immunology*
Transgenes / immunology
Grant Support
ID/Acronym/Agency:
AI39535/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Immunoglobulin Constant Regions; 0/Immunoglobulin Heavy Chains; 0/Immunoglobulin Light Chains; 0/Receptors, Antigen, B-Cell

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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