CD34+fibrocytes in neoplastic and inflammatory pancreatic lesions
CD34+fibrocytes in neoplastic and inflammatory pancreatic lesions
复制标题
DOI：
10.1007/s00428-001-0551-3
复制
发表时间：
2002-02-01
期刊：
影响因子：
3.5
通讯作者：
Ramaswamy, A
中科院分区：
文献类型：
--
作者：
Barth, PJ;Ebrahimsade, S;Ramaswamy, A
除了作为基质生成细胞的功能外，CD34（+）纤维细胞已被报道为一种抗原呈递细胞，能够原位启动初始T细胞。因此，CD34（+）纤维细胞可能在宿主对组织损伤的应答中起重要作用。本研究的目的是分析CD34（+）纤维细胞和平滑肌肌动蛋白（SMA）反应性肌成纤维细胞的存在和分布与潜在胰腺疾病的关系。我们共研究了12例胰腺腺癌、7例胰腺内分泌肿瘤和8例慢性胰腺炎；11例胰腺组织正常。正常胰腺组织间质含有弥漫性分散的CD34（+）纤维细胞。慢性胰腺炎的特征是间质CD34（+）纤维细胞数量增加，并伴有SMA反应性肌成纤维细胞的增加，这在正常胰腺间质中没有观察到。胰腺导管腺癌和内分泌肿瘤的间质中缺乏CD34（+）纤维细胞或至少局部缺失这种细胞类型，而在内分泌肿瘤和腺癌中均检测到SMA反应性肌成纤维细胞。我们的结论是，检测CD34（+）纤维细胞可能是区分慢性胰腺炎和导管腺癌的辅助工具，因为缺乏这种细胞群强烈倾向于肿瘤过程。此外，CD34（+）纤维细胞和肌成纤维细胞似乎参与了与慢性胰腺炎和导管腺癌相关的基质重塑。
Besides its function as a matrix-producing cell, the CD34(+) fibrocyte has been reported to be an antigen-presenting cell capable of priming naive T cells in situ. Therefore, it has been claimed that the CD34(+) fibrocyte may play an important role in host response to tissue damage. The objective of the present study was to analyze the presence and distribution of CD34(+) fibrocytes and smooth muscle actin (SMA) reactive myofibroblasts in relation to the underlying pancreatic disease. We investigated a total of 12 pancreatic adenocarcinomas, 7 endocrine tumors of the pancreas, and 8 cases of chronic pancreatitis; in 11 cases, normal pancreatic tissue was available. The stroma of normal pancreatic tissue harbored diffusely scattered CD34(+) fibrocytes. Chronic pancreatitis was characterized by an increased number of stromal CD34(+) fibrocytes paralleled by a gain of SMA reactive myofibroblasts which were not observed in the normal pancreatic stroma. The stroma of pancreatic ductal adenocarcinomas and endocrine tumors was devoid of CD34(+) fibrocytes or showed at least a focal loss of this cell type, whereas SMA reactive myofibroblasts were detected in both endocrine tumors and adenocarcinomas. We conclude that detection of CD34(+) fibrocytes may constitute an adjunctive tool in distinguishing chronic pancreatitis from ductal adenocarcinoma since the absence of this cell population strongly favors a neoplastic process. Moreover, CD34(+) fibrocytes and myofibroblasts appear to be involved in stromal remodeling associated with chronic pancreatitis and ductal adenocarcinoma.