Publikationsdatum:
2002-12-21
Beschreibung:
The immunoglobulin G (IgG)-containing B lymphocyte antigen receptor (IgG-BCR) transmits a signal distinct from that of IgM-BCR or IgD-BCR, although all three use the same signal-transducing component, Igalpha/Igbeta. Here we demonstrate that the inhibitory coreceptor CD22 down-modulates signaling through IgM-BCR and IgD-BCR, but not that through IgG-BCR, because of the IgG cytoplasmic tail, which prevents CD22 phosphorylation. These results suggest that the cytoplasmic tail of IgG specifically enhances IgG-BCR signaling by preventing CD22-mediated signal inhibition. Enhanced signaling through IgG-BCR may be involved in efficient IgG production, which is crucial for immunity to pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wakabayashi, Chisato -- Adachi, Takahiro -- Wienands, Jurgen -- Tsubata, Takeshi -- New York, N.Y. -- Science. 2002 Dec 20;298(5602):2392-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Medical Research Institute, Tokyo Medical and Dental University, 113-8510 Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12493916" target="_blank"〉PubMed〈/a〉
Schlagwort(e):
Animals
;
Antigens, CD/metabolism
;
Antigens, Differentiation, B-Lymphocyte/metabolism
;
B-Lymphocytes/immunology/metabolism
;
Calcium/metabolism
;
Calcium Signaling
;
*Cell Adhesion Molecules
;
Cells, Cultured
;
Immunoglobulin D/immunology/metabolism
;
Immunoglobulin G/chemistry/immunology/*metabolism
;
Intracellular Signaling Peptides and Proteins
;
Lectins/metabolism
;
Mice
;
Mitogen-Activated Protein Kinase 1/metabolism
;
Mitogen-Activated Protein Kinase 3
;
Mitogen-Activated Protein Kinases/metabolism
;
Phosphorylation
;
Protein Tyrosine Phosphatase, Non-Receptor Type 6
;
Protein Tyrosine Phosphatases/metabolism
;
Receptors, Antigen, B-Cell/chemistry/immunology/*metabolism
;
Sialic Acid Binding Ig-like Lectin 2
;
*Signal Transduction
;
Transfection
;
Tumor Cells, Cultured
Print ISSN:
0036-8075
Digitale ISSN:
1095-9203
Thema:
Biologie
,
Chemie und Pharmazie
,
Informatik
,
Medizin
,
Allgemeine Naturwissenschaft
,
Physik
Permalink