Curbing Inflammation in Multiple Sclerosis and Endometriosis: Should Mast Cells Be Targeted?

Figure 1

Mast cells mediated inflammation and fibrosis. Mast cells circulate as CD34-positive precursor cells and terminally differentiate in connective tissues. Both IgE dependent and independent mechanisms can activate mast cells causing the release of preformed and newly synthesized proinflammatory mediators. Many of these mediators increase vascular permeability and promote the recruitment of other inflammatory cells and additional mast cell precursors. SCF is also secreted by activated fibroblasts and myofibroblasts, further potentiating mast cell recruitment and proliferation. TGF-β is a potent fibroblast mitogen and stimulator of myofibroblast differentiation. It also impedes myofibroblasts apoptosis. bFGF, basic fibroblast growth factor; CGRP, calcitonin gene-related peptide; CTGF, connective tissue growth factor; NGF, nerve growth factor; PDGF, platelet-derived growth factor; SCF, stem cell factor; TGF-β, transforming growth factor-beta; TNF-α, tumor necrosis factor-alpha; VIP, vasoactive intestinal peptide. This figure was reproduced from [19].