Lacour J P, Vitetta A, Chiquet-Ehrismann R, Pisani A, Ortonne J P
Department of Dermatology, University of Nice, France.
Br J Dermatol. 1992 Oct;127(4):328-34. doi: 10.1111/j.1365-2133.1992.tb00450.x.
The expression of tenascin, a recently discovered extracellular matrix protein, was studied by immunohistochemical techniques in scleroderma skin and compared with its distribution in normal skin. In progressive systemic sclerosis, a marked increase in tenascin content was observed in the superficial reticular dermis. In localized scleroderma, the deposition of tenascin was increased both in the superficial and deep dermis of involved skin, whereas in clinically uninvolved skin the distribution of tenascin was the same as in normal control skin, i.e. the papillary dermis and peri-appendiceal zone. The distribution of tenascin did not strictly parallel that of fibronectin. These findings and the current knowledge of tenascin biology suggest that the overproduction of tenascin in scleroderma dermis could be secondary to stimulation of fibroblasts by immune cell-derived cytokines, or could be due to abnormal fibroblasts, or a subpopulation of fibroblasts, producing high levels of this extracellular matrix protein.
采用免疫组织化学技术研究了近期发现的细胞外基质蛋白肌腱蛋白在硬皮病皮肤中的表达，并将其与正常皮肤中的分布进行了比较。在进行性系统性硬化症中，在浅表网状真皮中观察到肌腱蛋白含量显著增加。在局限性硬皮病中，受累皮肤的浅表和深部真皮中肌腱蛋白的沉积均增加，而在临床上未受累的皮肤中，肌腱蛋白的分布与正常对照皮肤相同，即乳头真皮和阑尾周围区域。肌腱蛋白的分布与纤连蛋白并不严格平行。这些发现以及目前对肌腱蛋白生物学的认识表明，硬皮病真皮中肌腱蛋白的过度产生可能继发于免疫细胞衍生的细胞因子对成纤维细胞的刺激，或者可能是由于产生这种细胞外基质蛋白水平高的异常成纤维细胞或成纤维细胞亚群所致。
