The mast cell is related, but not identical, to the basophil, a white blood cell that contains similar granules (Table 6.6). They both arise from a pluripotential hemopoietic stem cell (HSC) in the bone marrow. Mast cells initially circulate in the peripheral blood as agranular cells of monocytic appearance. After migrating into the connective tissue, immature mast cells differentiate and produce their characteristic granules (Fig. 6.23b). In contrast, basophils differentiate and remain within the circulatory system. The surface of mature mast cells express a large number of high-affinity Fc receptors (Fc RI) to which immunoglobulin E (IgE) antibodies are attached. Binding of specific antigen to exposed IgE antibody molecules on the mast cell surface leads to an aggregation of Fc receptors.
 FOLDER 6.3 Clinical Correlations: Role of Myofibroblasts in Wound Repair cess of wound healing. A clean surgical skin incision begins the healing process when a blood clot containing fibrin and blood cells fill the narrow space between the edges of the incision. The infammatory process, which begins as early as 24 hours after initial injury, contains the damage to a small area, aids in the removal of injured and dead tissues, and initiates deposition of new ECM proteins. During the initial phases of inflammation, neutrophils and monocytes infiltrate the injury (maximum infiltration by neutrophils occurs in the first 1 to 2 days after injury). Monocytes transform into macrophages (they usually replace neutrophils by day 3 after injury) (page 181). At the same time, in response to local growth factors, fibroblasts and vascular endothelial cells begin to proliferate and migrate into the delicate fibrin matrix of the blood clot, forming the granulation tissue, a specialized type of tissue characteristic of the repair process. Usually by day 5 after injury, the fully developed granulation tissue bridges the incision gap. It is composed mainly of large numbers of small vessels, fibroblasts, and myofibroblasts, and variable numbers of other inflammatory cells. Migra ting fibroblasts exert tractional forces on the ECM, reorganizing it along lines of stress. Under the influence of growth factors such as TGF-1 and mecha nical forces, fibro blasts undergo differentiation into myofbroblasts.This -SMA. This type of actin is not present in the cytoplasm of fibroblasts (Fig. 6.3.1). The myofibroblasts generate and maintain steady contractile force (similar to that of smooth muscle cells) that cause shortening of the connective tissue fibers and wound closure. At the same time, myofibroblasts synthesize and lay down collagen fibers and other ECM components that are responsible for tissue remodeling. During the second week of wound healing, the amount of cells in tissue undergoing repair decreases; most of the myofibroblasts undergo apoptosis and disappear, resulting in a connective scar that has very few cellular elements. In some pathologic conditions, myofibroblasts persist and continue the process of remodeling. This continued remodeling causes hypertrophic scar formation, resulting in excessive connective tissue contracture. Extensive numbers of myofibroblasts are found in most contractive diseases of connective tissue (fibromatoses). For example, palmar fbromatosis (Dupuytren’s disease) is characterized by the thickening of palmar aponeurosis, which leads to progressive flex-ion contracture of the fourth and fifth digits of the hand (Fig. F 6.3.2) If scar tissue grows beyond boundaries of the original wound and does not regress, it is called a keloid. Its formation is more common among African Americans than other ethnic groups.