Salivary gland expression of transforming growth factor beta isoforms in Sjogren's syndrome and benign lymphoepithelial lesions.

G I Mason, J Hamburger, S Bowman, J B Matthews
{"title":"Salivary gland expression of transforming growth factor beta isoforms in Sjogren's syndrome and benign lymphoepithelial lesions.","authors":"G I Mason, J Hamburger, S Bowman, J B Matthews","doi":"10.1136/mp.56.1.52","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>Transforming growth factor beta (TGF-beta) is involved in the control of autoimmune reactions, cell proliferation, and the accumulation of lymphocytes within organs. The aim of this study was to determine the expression of TGF-beta in salivary glands from patients with primary Sjogren's syndrome (SS) and benign lymphoepithelial lesions (BLEL) with emphasis on ductal epithelium.</p><p><strong>Methods: </strong>Immunoperoxidase staining for TGF-beta isoforms and Ki67 antigen was performed on formalin fixed sections of labial glands from patients with primary SS (n = 15) and controls (n = 5) and parotid glands reported as BLEL (n = 5) or normal (n = 5). Ductal expression of TGF-beta was quantified by absorbance measurements using image analysis. The specificity of staining was confirmed by peptide blocking studies.</p><p><strong>Results: </strong>All TGF-beta isoforms were detected within the cytoplasm of most lymphocytes, endothelial cells, and ducts in all specimens. Acinar expression was variable and weaker than that seen in ducts. Absorbance measurements revealed that the expression of all isoforms was greater in ducts within primary SS glands than in control glands. Ductal expression in control parotid glands was greater than that seen in BLEL glands, irrespective of the presence of adjacent lymphoid infiltrates. Comparisons between control specimens showed that ductal expression of all isoforms was highest in parotid glands, whereas no differences were detected between primary SS and BLEL glands. Ki67 positive lymphocytes and duct cells were mainly restricted to pathological specimens, with BLEL glands containing larger populations of positive cells than primary SS glands.</p><p><strong>Conclusion: </strong>These results demonstrate complex and variable changes in ductal expression of TGF-beta in primary SS and BLEL, which may be important in the control of lymphoid infiltration and the proliferation of lymphocytes and ductal epithelium.</p>","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 1","pages":"52-9"},"PeriodicalIF":0.0000,"publicationDate":"2003-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1187290/pdf/mp56000052.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular pathology : MP","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1136/mp.56.1.52","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Aim: Transforming growth factor beta (TGF-beta) is involved in the control of autoimmune reactions, cell proliferation, and the accumulation of lymphocytes within organs. The aim of this study was to determine the expression of TGF-beta in salivary glands from patients with primary Sjogren's syndrome (SS) and benign lymphoepithelial lesions (BLEL) with emphasis on ductal epithelium.

Methods: Immunoperoxidase staining for TGF-beta isoforms and Ki67 antigen was performed on formalin fixed sections of labial glands from patients with primary SS (n = 15) and controls (n = 5) and parotid glands reported as BLEL (n = 5) or normal (n = 5). Ductal expression of TGF-beta was quantified by absorbance measurements using image analysis. The specificity of staining was confirmed by peptide blocking studies.

Results: All TGF-beta isoforms were detected within the cytoplasm of most lymphocytes, endothelial cells, and ducts in all specimens. Acinar expression was variable and weaker than that seen in ducts. Absorbance measurements revealed that the expression of all isoforms was greater in ducts within primary SS glands than in control glands. Ductal expression in control parotid glands was greater than that seen in BLEL glands, irrespective of the presence of adjacent lymphoid infiltrates. Comparisons between control specimens showed that ductal expression of all isoforms was highest in parotid glands, whereas no differences were detected between primary SS and BLEL glands. Ki67 positive lymphocytes and duct cells were mainly restricted to pathological specimens, with BLEL glands containing larger populations of positive cells than primary SS glands.

Conclusion: These results demonstrate complex and variable changes in ductal expression of TGF-beta in primary SS and BLEL, which may be important in the control of lymphoid infiltration and the proliferation of lymphocytes and ductal epithelium.

Sjogren's 综合征和良性淋巴上皮病变中唾液腺转化生长因子 beta 同工酶的表达。
目的:转化生长因子 beta(TGF-beta)参与控制自身免疫反应、细胞增殖和淋巴细胞在器官内的聚集。本研究旨在确定原发性斯约格伦综合征(SS)和良性淋巴上皮病变(BLEL)患者唾液腺中 TGF-beta 的表达情况,重点是导管上皮:方法:对原发性 Sjogren's 综合征患者(15 例)和对照组(5 例)唇腺的福尔马林固定切片以及报告为 BLEL(5 例)或正常(5 例)的腮腺切片进行 TGF-beta 同工酶和 Ki67 抗原的免疫过氧化物酶染色。TGF-beta在导管中的表达通过图像分析的吸光度测量进行量化。多肽阻断研究证实了染色的特异性:结果:在所有标本中,大多数淋巴细胞、内皮细胞和导管的细胞质中都检测到了所有 TGF-beta 同工型。渐开线的表达不一,且弱于导管中的表达。吸光测量显示,原发性 SS 腺体内导管中所有同工酶的表达均高于对照腺体。对照组腮腺中导管的表达高于BLEL腺体,与邻近淋巴浸润的存在无关。对照标本之间的比较显示,腮腺中所有同工酶的导管表达量最高,而原发性SS腺和BLEL腺之间没有发现差异。Ki67阳性淋巴细胞和导管细胞主要局限于病理标本,BLEL腺体比原发性SS腺体含有更多的阳性细胞:这些结果表明,原发性 SS 和 BLEL 的导管中 TGF-beta 的表达发生了复杂多变的变化,这可能是控制淋巴细胞浸润以及淋巴细胞和导管上皮增殖的重要因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信