Telocytes in minor salivary glands of primary Sjögren's syndrome: association with the extent of inflammation and ectopic lymphoid neogenesis.
Telocytes in minor salivary glands of primary Sjögren's syndrome: association with the extent of inflammation and ectopic lymphoid neogenesis.
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DOI：
10.1111/jcmm.12545
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发表时间：
2015-07
影响因子：
5.3
通讯作者：
Manetti M
中科院分区：
文献类型：
--
作者：
Alunno A;Ibba-Manneschi L;Bistoni O;Rosa I;Caterbi S;Gerli R;Manetti M
最近有报道称，端粒细胞是一种基质(间质)细胞亚群，参与控制局部组织的动态平衡，在炎症/自身免疫疾病的靶器官中受到阻碍。由于目前还没有关于小涎腺(MSG)中端粒细胞的数据，本研究的目的是评估端粒细胞在结构正常的MSG、非特异性慢性涎腺炎(NSCS)和原发性干燥综合征(PSS)局灶性淋巴细胞性涎腺炎中的分布。12例PSS患者和16例SICCA非PSS受试者纳入研究。采用苏木精-伊红染色和CD3/CD20、CD21免疫荧光染色方法，评价病灶评分、Tarpley活检评分、T/B细胞分离和生发中心(GC)样结构。采用免疫组织化学法检测CD34和CD34/血小板衍生生长因子受体α双重免疫荧光标记端粒细胞。正常MSG的间质中有大量的端粒细胞，其长的胞质突起包围着血管，包围着排泄管和分泌单位。在NSCS中，尽管存在一定程度的炎症，但端粒细胞正常表达。相反，PSS患者的MSG与正常和NSCS MSG相比，端粒细胞显著减少。这种减少与腺体炎症的恶化和异位淋巴样新生的进展有关，导管周围的端细胞在存在较小的炎症灶时减少，而在存在GC样结构时完全消失。我们的发现表明，味精端粒细胞的丢失可能在PSS中具有重要的病理生理学意义。PSS msgs特有的促炎细胞因子环境可能是导致端粒细胞丢失的原因之一。
It has been recently reported that telocytes, a stromal (interstitial) cell subset involved in the control of local tissue homeostasis, are hampered in the target organs of inflammatory/autoimmune disorders. Since no data concerning telocytes in minor salivary glands (MSGs) are currently available, aim of the study was to evaluate telocyte distribution in MSGs with normal architecture, non-specific chronic sialadenitis (NSCS) and primary Sjögren’s syndrome (pSS)-focal lymphocytic sialadenitis. Twelve patients with pSS and 16 sicca non-pSS subjects were enrolled in the study. MSGs were evaluated by haematoxylin and eosin staining and immunofluorescence for CD3/CD20 and CD21 to assess focus score, Tarpley biopsy score, T/B cell segregation and germinal center (GC)-like structures. Telocytes were identified by immunoperoxidase-based immunohistochemistry for CD34 and CD34/platelet-derived growth factor receptor α double immunofluorescence. Telocytes were numerous in the stromal compartment of normal MSGs, where their long cytoplasmic processes surrounded vessels and encircled both the excretory ducts and the secretory units. In NSCS, despite the presence of a certain degree of inflammation, telocytes were normally represented. Conversely, telocytes were markedly reduced in MSGs from pSS patients compared to normal and NSCS MSGs. Such a decrease was associated with both worsening of glandular inflammation and progression of ectopic lymphoid neogenesis, periductal telocytes being reduced in the presence of smaller inflammatory foci and completely absent in the presence of GC-like structures. Our findings suggest that a loss of MSG telocytes might have important pathophysiological implications in pSS. The specific pro-inflammatory cytokine milieu of pSS MSGs might be one of the causes of telocyte loss.