Ritter Matthew R, Reinisch John, Friedlander Sheila Fallon, Friedlander Martin
Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Am J Pathol. 2006 Feb;168(2):621-8. doi: 10.2353/ajpath.2006.050618.
Little is known about the pathogenesis of infantile hemangiomas despite the fact that they are relatively common tumors. These benign neoplasms occur in as many as 1 in 10 births, and although rarely life threatening, hemangiomas can pose serious concerns to the cosmetic and psychosocial development of the afflicted child. Ulceration, scarring, and disfigurement are significant problems as are encroachment of the ear and eye, which can threaten hearing and vision. The precise mechanisms controlling the rapid growth observed in the first months of life and the spontaneous involution that follows throughout the course of years remain unknown. In this report we demonstrate the presence of large numbers of hematopoietic cells of the myeloid lineage in proliferating hemangiomas and propose a mechanism for the observed evolution of these lesions that is triggered by hypoxia and involves the participation of myeloid cells. We report the results of experiments using myeloid markers (CD83, CD32, CD14, CD15) that unexpectedly co-labeled hemangioma endothelial cells, providing new evidence that these cells are distinct from normal endothelium.
尽管婴儿血管瘤是相对常见的肿瘤,但其发病机制却鲜为人知。这些良性肿瘤在每10例出生婴儿中就有1例出现,虽然很少危及生命,但血管瘤会给患病儿童的外貌和心理社会发育带来严重问题。溃疡、瘢痕形成和毁容是严重问题,耳部和眼部受侵犯也会威胁听力和视力。在生命最初几个月观察到的血管瘤快速生长以及随后数年的自然消退的精确控制机制仍然未知。在本报告中,我们证明增殖性血管瘤中存在大量髓系造血细胞,并提出了一种由缺氧触发且涉及髓系细胞参与的这些病变观察到的演变机制。我们报告了使用髓系标志物(CD83、CD32、CD14、CD15)的实验结果,这些标志物意外地共同标记了血管瘤内皮细胞,为这些细胞不同于正常内皮细胞提供了新证据。