The role of the lectin KM+ in mast cell activation

Abstract

Mast cells are immunoregulatory cells that participate in inflammatory processes, atopic diseases such as asthma, rhinitis, eczema and food allergies, and in the host defense mechanisms. In addition, they play important roles in tissue repair, angiogenesis and wound healing. These phenomena are directly related to the release of chemical mediators that occurs upon mast cell activation and degranulation. The major pathway of activating mast cells involves engagement of the high affinity receptor for IgE (FcERI) by the multivalent antigen (allergen).Lectin-carbohydrate interactions are able to induce mast cell activation. The D-mannose binding lectin KM+ induces mast cell degranulation. Mediators released by mast cells play a role in inflammatory processes and provide an ampliflication loop for the neutrophil recruitment to the rat peritoneal cavity induced by the lectin. In addition, KM+ acts on tissue repair and is able to protect against infection by Leishmania major and P. brasiliensis, where cell recruitment and the presence of mediators are essential. The mechanisms involved in KM+ induced mast cell degranulation remain unknown. Our preliminary data suggest that KM+ binds, through its CRDs, to FcERI or to FcERI bound IgE. The present work is undertaken to identify the KM+ ligand (s) on mast cell surface and to study the resulting cell activation events. Our increase in the knowledge of the events regulating mast cell activation and degranulation is important to delineate novel approaches for therapeutic interventions in allergic inflammatory diseases. (AU)