Document Detail


Developmental acquisition of the Lyn-CD22-SHP-1 inhibitory pathway promotes B cell tolerance.
MedLine Citation:
PMID:  19380785     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To better understand whether autoimmunity in Lyn-deficient mice arises from compromised central or peripheral B cell tolerance, we examined BCR signaling properties of wild-type and Lyn-deficient B cells at different stages of development. Wild-type mature follicular B cells were less sensitive to BCR stimulation than were immature transitional stage 1 B cells with regard to BCR-induced calcium elevation and ERK MAPK activation. In the absence of Lyn, mature B cell signaling was greatly enhanced, whereas immature B cell signaling was minimally affected. Correspondingly, Lyn deficiency substantially enhanced the sensitivity of mature B cells to activation via the BCR, but minimally affected events associated with tolerance induction at the immature stage. The effects of CD22 deficiency on BCR signaling were very similar in B cells at different stages of maturation. These results indicate that the Lyn-CD22-Src homology region 2 domain-containing phosphatase-1 inhibitory pathway largely becomes operational as B cell mature, and sets a threshold for activation that appears to be critical for the maintenance of tolerance in the B cell compartment.
Authors:
Andrew J Gross; Julia R Lyandres; Anil K Panigrahi; Eline T Luning Prak; Anthony L DeFranco
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  182     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2009 May 
Date Detail:
Created Date:  2009-04-21     Completed Date:  2009-06-15     Revised Date:  2014-09-10    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5382-92     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
B-Lymphocyte Subsets / cytology,  enzymology,  immunology*,  metabolism
Cell Differentiation / genetics,  immunology
Gene Expression Regulation, Developmental / physiology*
Immune Tolerance* / genetics
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Mutant Strains
Mice, Transgenic
Protein Tyrosine Phosphatase, Non-Receptor Type 6 / deficiency,  genetics*,  physiology
Receptors, Antigen, B-Cell / antagonists & inhibitors*,  genetics,  physiology
Sialic Acid Binding Ig-like Lectin 2 / genetics*,  metabolism,  physiology
Signal Transduction / genetics,  immunology*
Spleen / cytology,  enzymology,  immunology
Up-Regulation / genetics,  immunology
src-Family Kinases / deficiency,  genetics*,  physiology
Grant Support
ID/Acronym/Agency:
K08 AI52249/AI/NIAID NIH HHS; R01 AI020038/AI/NIAID NIH HHS; R01 AI020038-25/AI/NIAID NIH HHS; R01 AI20038/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Cd22 protein, mouse; 0/Receptors, Antigen, B-Cell; 0/Sialic Acid Binding Ig-like Lectin 2; EC 2.7.10.2/lyn protein-tyrosine kinase; EC 2.7.10.2/src-Family Kinases; EC 3.1.3.48/Protein Tyrosine Phosphatase, Non-Receptor Type 6; EC 3.1.3.48/Ptpn6 protein, mouse
Comments/Corrections

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


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