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干燥综合征和慢性涎腺炎患者小涎腺中细胞因子及黏附分子的表达

Cytokine and adhesion molecule expression in the minor salivary glands of patients with Sjögren's syndrome and chronic sialoadenitis.

作者信息

Cauli A, Yanni G, Pitzalis C, Challacombe S, Panayi G S

机构信息

Rheumatology Unit, United Medical School, Guy's Hospital, London, United Kingdom.

出版信息

Ann Rheum Dis. 1995 Mar;54(3):209-15. doi: 10.1136/ard.54.3.209.

DOI:10.1136/ard.54.3.209
PMID:7748018
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1005558/
Abstract

OBJECTIVE

To investigate the role of cytokines and cell adhesion molecules in the pathogenesis of Sjögren's syndrome (SS).

METHODS

Using an indirect immunoperoxidase technique we assessed the expression of the cytokines interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-8 (IL-8), transforming growth factor beta (TGF beta) and granulocyte macrophage colony stimulating factor (GM-CSF), of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), lymphocyte function associated antigen-1 (LFA-1), the activated molecular form of LFA-1 (NKI-L16), CD2, and LFA-3, and of a panel of cellular markers in the minor salivary glands.

RESULTS

In SS and chronic sialoadenitis (CS), the ductal epithelial cells and acini expressed all the cytokines examined. The percentage of glandular mononuclear cells which stained positive for cytokines did not differ significantly between SS and CS. NKI-L16 was detected on 33.6 (SD 10.1)% and 15.3 (4.3)% of LFA-1 cells in SS and CS, respectively (p < 0.002).

CONCLUSION

SS and CS did not differ in the pattern of cytokines examined. The characteristic cell clustering seen in the salivary glands in SS may be caused by the upregulation of NKI-L16.

摘要

目的

研究细胞因子和细胞黏附分子在干燥综合征(SS)发病机制中的作用。

方法

我们采用间接免疫过氧化物酶技术评估了细胞因子白细胞介素-1α(IL-1α)、白细胞介素-1β(IL-1β)、白细胞介素-8(IL-8)、转化生长因子β(TGFβ)和粒细胞巨噬细胞集落刺激因子(GM-CSF),黏附分子细胞间黏附分子-1(ICAM-1)、淋巴细胞功能相关抗原-1(LFA-1)、LFA-1的活化分子形式(NKI-L16)、CD2和淋巴细胞功能相关抗原3(LFA-3),以及一组细胞标志物在小唾液腺中的表达。

结果

在SS和慢性涎腺炎(CS)中,导管上皮细胞和腺泡表达了所有检测的细胞因子。SS和CS中细胞因子染色阳性的腺性单核细胞百分比无显著差异。在SS和CS中,分别有33.6(标准差10.1)%和15.3(4.3)%的LFA-1细胞检测到NKI-L16(p<0.002)。

结论

SS和CS在所检测的细胞因子模式上无差异。SS唾液腺中所见的特征性细胞聚集可能由NKI-L16上调引起。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/1005558/8e6f0e570962/annrheumd00503-0057-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/1005558/6f1662cddf8d/annrheumd00503-0055-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/1005558/8e6f0e570962/annrheumd00503-0057-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/1005558/6f1662cddf8d/annrheumd00503-0055-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/1005558/8e6f0e570962/annrheumd00503-0057-a.jpg

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