Abstract:
:Mature B cells express a single immunoglobulin Fc receptor, FcgammaRIIB, that functions to block downstream signaling by co-aggregated antigen receptors. Co-aggregation of receptors is essential because BCR activated kinases must phosphorylate FcgammaRIIB to recruit SHIP and mediate inhibitory signals. Pre-B cells also express FcgammaRIIB, but since they do not yet express antigen receptor, it is unclear when they are activated physiologically. Here, we demonstrate that aggregation of the FcR on pre-B cells leads to potent inhibitory signaling. Aggregation of the FcR alone leads to downstream effects including the induction of cell death and the blockade of SDF-1 induced migration. The biochemical circuitry that mediates this response is unique because although SHIP is required for this signaling and is phosphorylated upon receptor aggregation, this occurs in the absence of FcgammaRIIB phosphorylation. Results indicate that immune complexes may inhibit B cell production in the bone marrow by antigen non-specific mechanisms.
journal_name
Immunol Lettjournal_title
Immunology lettersauthors
Brauweiler AM,Cambier JCdoi
10.1016/j.imlet.2003.11.028subject
Has Abstractpub_date
2004-03-29 00:00:00pages
75-81issue
1-2eissn
0165-2478issn
1879-0542pii
S0165247803003031journal_volume
92pub_type
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pub_type: 杂志文章,meta分析,评审
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