Ding D, Dong Y, Li S
Peking Union Medical College Hospital, Beijing.
Zhonghua Yi Xue Za Zhi. 1996 Jun;76(6):427-30.
To explore the role of cytokines in the process of inflammation and destruction of minor salivary gland in Sjögren's Syndrome. (SS) METHODS: Using in situ non-isotope double hybridization method, we detected the mRNA of the following cytokines: TNF alpha, IL-1 beta, IL-6, PDGF alpha and PDGF beta in 24 labial gland biopsied sections.
No cytokine could be detected in the normal labial glands sections. The positivity of all cytokine expression was higher in the pSS and sSS patients than that in the control. The intensity of TNF alpha expression was 3-4 fold increase in pSS compared with sSS. The different cytokines were expressed with the different grade of lymphocytic focus. The site of different cytokines was also expressed differently. The coexpression of mRNA of TNF alpha and IL-1 beta or TNF alpha and IL-6 was only seen in the inflammatory mononuclear cells but not others. The expression of TNF alpha in aciniar cells could occur earlier than the infiltration of lymphocytes in the interstitial region. It was found that the IL-6 positive group had higher positivity of serum ANA compared with the IL-6 negative group according to Ridit statistical analysis (P < 0.05). The serum anti-SSA and anti-SSB antibody had an increase tendency in the IL-6 positive group.
We hypothesize that the development of SS may be secondary to some trigger agents, which activated the aciniar cells in exocrine gland of predisposed individuals. The activated acini cells secreted TNF alpha, then TNF alpha induced other cytokine expression, followed by the lymphocytes infiltration, which led to autoimmne reaction and the destruction of the exocrine gland.
探讨细胞因子在干燥综合征(SS)患者小唾液腺炎症及破坏过程中的作用。方法:采用原位非同位素双杂交法,检测24例唇腺活检组织切片中下列细胞因子的mRNA:肿瘤坏死因子α(TNFα)、白细胞介素1β(IL-1β)、白细胞介素6(IL-6)、血小板衍生生长因子α(PDGFα)和血小板衍生生长因子β(PDGFβ)。
正常唇腺组织切片未检测到细胞因子。原发性干燥综合征(pSS)和继发性干燥综合征(sSS)患者所有细胞因子表达的阳性率均高于对照组。与sSS相比,pSS中TNFα表达强度增加3 - 4倍。不同细胞因子在不同程度的淋巴细胞灶中表达不同。不同细胞因子的表达部位也有所不同。TNFα与IL-1β或TNFα与IL-6的mRNA共表达仅见于炎性单核细胞,其他细胞未见。腺泡细胞中TNFα的表达可早于间质区淋巴细胞浸润。经Ridit统计分析发现,IL-6阳性组血清抗核抗体(ANA)阳性率高于IL-6阴性组(P < 0.05)。IL-6阳性组血清抗SSA和抗SSB抗体有升高趋势。
我们推测,SS的发病可能继发于某些触发因素,这些因素激活了易感个体外分泌腺中的腺泡细胞。活化的腺泡细胞分泌TNFα,然后TNFα诱导其他细胞因子表达,随后淋巴细胞浸润,导致自身免疫反应和外分泌腺破坏。