A newly recognized pathway for the negative regulation of mast cell-dependent hypersensitivity and inflammation mediated by an endogenous cell surface receptor of the gp49 family.
Mast cells are constitutively present at the portals between self and nonself, and contain a large and diverse complement of proinflammatory mediators. These characteristics suggest that the activation of mast cells must be carefully regulated in vivo. Regulation of pathologic and physiologic mast cell activation has been traditionally associated simply with the presence or absence of an activating signal. We examine here evidence supporting a new paradigm: mast cell homeostasis may result from inhibition of activation mediated by receptors on the surface of mast cells, typified by a member of the gp49 family.
Katz
H R
HR
Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115, USA. hkatz@warren.med.harvard.edu
Austen
K F
KF
D000595:Amino Acid Sequence; D000818:Animals; D000954:Antigens, Surface / Q000276:immunology*; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D008407:Mast Cells / Q000276:immunology*; D008562:Membrane Glycoproteins / Q000276:immunology*; D008969:Molecular Sequence Data; D011971:Receptors, Immunologic / Q000276:immunology*
D000954:Antigens, Surface; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic