title: Inhibition of anaphylactic inflammation by the gp49B1 receptor on mast cells.
abstract: gp49B1 is a member of the immunoglobulin (Ig) superfamily expressed on the surface of mast cells, macrophages, and activated natural killer cells. gp49B1 inhibits FcepsilonRI-induced activation of mast cells in vitro by virtue of two immunoreceptor, tyrosine-based inhibitory motifs that recruit the SHP-1 tyrosine phosphatase to the plasma membrane. We created gp49B1 null mice by targeted gene disruption, and found that IgE-dependent mast cell activation is augmented in these animals. Moreover, the ensuing anaphylactic reactions and inflammation are enhanced in the absence of gp49B1. Thus, gp49B1 innately counter-regulates mast cell activation mediated by Ig generated through the adaptive immune response in vivo.
authors.affiliation: Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA. hrkatz@mbcrr.harvard.edu
authors.forename: Howard R
authors.initials: HR
authors.lastname: Katz
mesh_terms: D000707:Anaphylaxis / Q000276:immunology*; D000818:Animals; D007249:Inflammation / Q000276:immunology; D008407:Mast Cells / Q000276:immunology*; D008562:Membrane Glycoproteins / Q000737:chemistry / Q000502:physiology*; D051379:Mice; D017434:Protein Structure, Tertiary; D011971:Receptors, Immunologic / Q000737:chemistry / Q000502:physiology*
chemical_list: C489447:Gp49a protein, mouse; C489448:Lilrb4 protein, mouse; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic