Document Detail

Increased NF-kappa B activity in B cells and bone marrow-derived dendritic cells from NOD mice.
MedLine Citation:
PMID:  15114673     Owner:  NLM     Status:  MEDLINE    
Type 1 diabetes results from the breakdown of peripheral tolerance. As regulators of T cell activation, antigen-presenting cells (APC) modulate peripheral tolerance and hence contribute to the immune dysregulation characteristic of insulin-dependent diabetes mellitus (IDDM). We initially observed an increased importance of NOD B cell APC function in a T cell priming assay as compared to non-autoimmune strains. Consistent with this increased APC function, we found that NF-kappa B nuclear translocation is increased in unmanipulated NOD and NOD.B10Sn-H2(b) B cells and that, in addition, NOD B cells are more sensitive to NF-kappa B-activating stimuli. We obtained similar results using NOD bone marrow-derived dendritic cell (BMDC) cultures. As costimulatory molecules have been shown to be NF-kappa B responsive, we examined the expression of these markers on NOD APC. Both B cells and BMDC expressed elevated levels of CD80 and CD40. Finally, NOD B cells provided better allostimulation than B cells from non-autoimmune strains. Therefore, hyperactivation of NF-kappa B and increased expression of CD80 and CD40 by NOD B cells and BMDC may be a contributing factor in the selection of effector T cells observed in IDDM.
William Wheat; Rene Kupfer; Diane G Gutches; Gina R Rayat; Joshua Beilke; Robert I Scheinman; Dale R Wegmann
Related Documents :
7543513 - Stimulation of germinal center b lymphocyte proliferation by an fdc-like cell line, hk.
22326293 - Role of leucine-rich pentatricopeptide repeat motif-containing protein (lrpprc) for ant...
24665413 - Hgf signaling regulates claudin-3 dynamics through its c-terminal tyrosine residues.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  European journal of immunology     Volume:  34     ISSN:  0014-2980     ISO Abbreviation:  Eur. J. Immunol.     Publication Date:  2004 May 
Date Detail:
Created Date:  2004-04-28     Completed Date:  2004-06-29     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  1273201     Medline TA:  Eur J Immunol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  1395-404     Citation Subset:  IM    
Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver, 80262, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Antigen-Presenting Cells / immunology
Autoantigens / immunology
B-Lymphocytes / immunology,  metabolism*
Bone Marrow Cells / metabolism
Cell Nucleus / metabolism
Dendritic Cells / metabolism*
Insulin / immunology
Membrane Proteins / immunology
Mice, Inbred NOD
NF-kappa B / metabolism*
Protein Tyrosine Phosphatase, Non-Receptor Type 1
Protein Tyrosine Phosphatases / immunology
Receptor-Like Protein Tyrosine Phosphatases, Class 8
T-Lymphocytes / immunology
Grant Support
Reg. No./Substance:
0/Autoantigens; 0/Membrane Proteins; 0/NF-kappa B; 11061-68-0/Insulin; EC protein, human; EC Tyrosine Phosphatase, Non-Receptor Type 1; EC Tyrosine Phosphatases; EC Protein Tyrosine Phosphatases, Class 8

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

Previous Document:  Perforin and IFN-gamma do not significantly regulate the virus-specific CD8+ T cell response in the ...
Next Document:  Inhibition of Notch signaling biases rat thymocyte development towards the NK cell lineage.