Mariana C. Castells, Lloyd B. Klickstein, Kevin Hassani, Jose A. Cumplido, Mario E. Lacouture, K. Frank Austen
& Howard R. Katz
Department of Medicine, Harvard Medical School and Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA.
We have identified the integrin v3 as a ligand for mouse gp49B1, thus identifying a new class of ligand for a member of the family of inhibitory immunoreceptors that bear C2-type immunoglobulin-like domains. The specific interaction was shown by both cell-protein and cell-cell binding assays. In addition, we found that the interaction of v3 with gp49B1 on bone marrow−derived mouse mast cells inhibited antigen-induced immunoglobulin E−mediated cell activation. Because neither gp49B1 nor v3 exhibit substantive allelic variation, their newly appreciated interaction may reflect an innate pathway for down-regulating the activity of mast cells.
v
3 interaction inhibits antigen-induced mast cell activation
v
3 as a ligand for mouse gp49B1, thus identifying a new class of ligand for a member of the family of inhibitory immunoreceptors that bear C2-type immunoglobulin-like domains. The specific interaction was shown by both cell-protein and cell-cell binding assays. In addition, we found that the interaction of 
