Mast Cell Deficiency, A Game of Kit and Mouse Howard R. Katz, K. Frank Austen  Immunity  Volume 35, Issue 5, Pages 668-670 (November 2011) DOI: 10.1016/j.immuni.2011.11.004 Copyright © 2011 Elsevier Inc. Terms and Conditions

Figure 1 Segregation of MC-Dependent and Additional Kit-Dependent Roles in Pathobiologic Responses Kit drives development of both the myeloid and lymphoid lineages from stem cells. Mast cell progenitors (MCps), defined by the indicated expression of cell surface markers, generate constitutive MCs in connective tissue (CTMCs) that contribute to local and systemic IgE-dependent anaphylaxis and hapten-driven contact hypersensitivity in the skin. Mast cells induced in mucosal tissues in response to Th2 cell-driven inflammation (MMCs) serve as effector cells of allergic inflammation and in the intestine contribute to clearance of helminths. In contrast, Kit-dependent cells other than MCs, including cells derived from lymphoid, myeloid, and nonhematopoietic lineages, appear to drive autoimmune inflammation typified by antibody-induced arthritis and experimental autoimmune encephalitis models, as well as basal airway hyperresponsiveness in naive A/J mice (Cozzi et al., 2011). HSC, hematopoietic stem cell. Immunity 2011 35, 668-670DOI: (10.1016/j.immuni.2011.11.004) Copyright © 2011 Elsevier Inc. Terms and Conditions