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.
机构:
Australian Natl Univ, John Curtin Sch Med Res, Med Genome Ctr, ACRF Genet Lab, Canberra, ACT 2601, AustraliaAustralian Natl Univ, John Curtin Sch Med Res, Med Genome Ctr, ACRF Genet Lab, Canberra, ACT 2601, Australia
Martin, SW
;
Goodnow, CC
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机构:
Australian Natl Univ, John Curtin Sch Med Res, Med Genome Ctr, ACRF Genet Lab, Canberra, ACT 2601, AustraliaAustralian Natl Univ, John Curtin Sch Med Res, Med Genome Ctr, ACRF Genet Lab, Canberra, ACT 2601, Australia
机构:
Australian Natl Univ, John Curtin Sch Med Res, Med Genome Ctr, ACRF Genet Lab, Canberra, ACT 2601, AustraliaAustralian Natl Univ, John Curtin Sch Med Res, Med Genome Ctr, ACRF Genet Lab, Canberra, ACT 2601, Australia
Martin, SW
;
Goodnow, CC
论文数: 0引用数: 0
h-index: 0
机构:
Australian Natl Univ, John Curtin Sch Med Res, Med Genome Ctr, ACRF Genet Lab, Canberra, ACT 2601, AustraliaAustralian Natl Univ, John Curtin Sch Med Res, Med Genome Ctr, ACRF Genet Lab, Canberra, ACT 2601, Australia