Low-dose MTX may act on psoriasis by suppressing the TNF-alpha-induced expression of ICAM-1 and VCAM-1 by vascular endothelial cells. Inhibition of neovascularization may be another mechanism of action of MTX.
We have previously shown that frontoparietal scleroderma en coup de sabre, a type of linear scleroderma that affects the face and scalp, follows the lines of Blaschko, but the question whether linear scleroderma that occurs in the limbs follows Blaschko's lines has not been answered. We describe the case of a 4-year-old girl with multiple morphea showing remarkable unilateral systematized distribution and whose linear lesions in the limbs appeared to follow Blaschko's lines. We suggest that linear scleroderma of the limbs, as well as frontoparietal scleroderma, may occur along the lines of Blaschko. Since both the unilateral distribution and the lesions along Blaschko's lines are the patterns created by genetic mosaicism, we suggest that a significant part of linear scleroderma and perhaps a smaller part of multiple morphea could be related to cutaneous mosaicism.
Stem cell factor is essential to the migration and differentiation of melanocytes during embryogenesis based on the observation that mutations in either the stem cell factor gene, or its ligand, KIT, result in defects in coat pigmentation in mice. Stem cell factor is also required for the survival of melanocyte precursors while they are migrating towards the skin. Transforming growth factor beta1 has been implicated in the regulation of both cellular proliferation and differentiation. NCC-melb4, an immortal cloned cell line, was cloned from a mouse neural crest cell. NCC-melb4 cells provide a model to study the specific stage of differentiation and proliferation of melanocytes. They also express KIT as a melanoblast marker. Using the NCC-melb4 cell line, we investigated the effect of transforming growth factor beta1 on the differentiation and proliferation of immature melanocyte precursors. Immunohistochemically, NCC-melb4 cells showed transforming growth factor beta1 expression. The anti-transforming growth factor beta1 antibody inhibited the cell growth, and downregulated the KIT protein and mRNA expression. To investigate further the activation of autocrine transforming growth factor beta1, NCC-melb4 cells were incubated in nonexogenous transforming growth factor beta1 culture medium. KIT protein decreased with anti-transforming growth factor beta1 antibody concentration in a concentration-dependent manner. We concluded that in NCC-melb4 cells, transforming growth factor beta1 promotes melanocyte precursor proliferation in autocrine and/or paracrine regulation. We further investigated the influence of transforming growth factor beta1 in vitro using a neural crest cell primary culture system from wild-type mice. Anti-transforming growth factor beta1 antibody decreased the number of KIT positive neural crest cell. In addition, the anti-transforming growth factor beta1 antibody supplied within the wild-type neural crest explants abolished the growth of the neural crest cell. These results indicate that transforming growth factor beta1 affect melanocyte precursor proliferation and differentiation in the presence of stem cell factor/KIT in an autocrine/paracrine manner.
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