Mast Cell Growth, Differentiation, and Death

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Abstract
Mast cells (MC) begin development in the bone marrow. Following initial lineage commitment, the cells move into the vasculature as a committed progenitor (MCp) that is poorly phenotypically defined, but appears to be an agranular cell lacking the high-affinity IgE receptor characteristic of the mature tissue-localized MC. Full maturation occurs after the cells move into the various tissues. In the mouse, MCp localizing in the connective tissues appear to differentiate into mature MC, whereas those localizing in the lung and mucosal compartment of the small intestine remain largely as committed MCp. Movement of the MCp into the small intestine is controlled by the α4β7 integrin, whereas the factors controlling movement into other tissues remain to be defined. Following an inflammatory stimulus, Th2-derived cytokines drive the maturation process of these MCps, leading to the mature mucosal MC hyperplasia associated with events such as an intestinal helminth infection and possibly human allergy such as asthma and rhinitis. The expanded MC number disappears as the stimulus resolves. Various routes are used in the resolution of the MC hyperplasia including apoptosis, shedding along with the villous epithelium, and recirculation back to the spleen for elimination. Unlike the reactive MC that appears in association with inflammation, the connective tissue-localized MC is a long-lived radiation-resistant cell, which appears to depend principally on the presence of stem cell factor (SCF) for its persistence.

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