In:
Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 96, No. 14 ( 1999-07-06), p. 8110-8115
Abstract:
Mast cells are well known for their harmful role in IgE-mediated hypersensitivity reactions, but their physiological role remains a mystery. Several recent studies have reported that mast cells play a critical role in innate immunity in mice by releasing tumor necrosis factor α (TNF-α) to recruit neutrophils to sites of enterobacterial infection. In some cases, the mast cell TNF-α response was triggered when these cells directly bound FimH on the surface of Escherichia coli . We have identified CD48, a glycosylphosphatidylinositol-anchored molecule, to be the complementary FimH-binding moiety in rodent mast cell membrane fractions. We showed that ( i ) pretreatment of mast cell membranes with antibodies to CD48 or phospholipase C inhibited binding of FimH + E. coli , ( ii ) FimH + E. coli but not a FimH − derivative bound isolated CD48 in a mannose-inhibitable manner, ( iii ) binding of FimH + bacteria to Chinese hamster ovary (CHO) cells was markedly increased when these cells were transfected with CD48 cDNA, and ( iv ) antibodies to CD48 specifically blocked the mast cell TNF-α response to FimH + E. coli. Thus, CD48 is a functionally relevant microbial receptor on mast cells that plays a role in triggering inflammation.
Type of Medium:
Online Resource
ISSN:
0027-8424
,
1091-6490
DOI:
10.1073/pnas.96.14.8110
Language:
English
Publisher:
Proceedings of the National Academy of Sciences
Publication Date:
1999
detail.hit.zdb_id:
209104-5
detail.hit.zdb_id:
1461794-8
SSG:
11
SSG:
12
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