4.5 Article

Decrease of blood dendritic cells and increase of tissue-infiltrating dendritic cells are involved in the induction of Sjogren's syndrome but not in the maintenance

期刊

CLINICAL AND EXPERIMENTAL IMMUNOLOGY
卷 159, 期 3, 页码 315-326

出版社

WILEY
DOI: 10.1111/j.1365-2249.2009.04071.x

关键词

cytokines; dendritic cells; Sjogren's syndrome

资金

  1. Japan Society for the Promotion of Science [11670466]
  2. Grants-in-Aid for Scientific Research [11670466] Funding Source: KAKEN

向作者/读者索取更多资源

We have demonstrated previously that, in primary Sjogren's syndrome (SS), immature myeloid dendritic cells (DCs) are decreased in blood and mature myeloid DCs are accumulated in salivary glands, suggesting recruitment of the myeloid DCs from blood to salivary glands. To verify whether this finding is universal in patients of not only primary SS but also secondary SS, in this study we analysed the blood DCs of secondary SS patients. We examined 24 secondary SS and 29 primary SS patients. A direct correlation between the decreased number of myeloid DCs and the duration of Sicca syndrome in primary and secondary SS was observed; namely, the reduction of myeloid DCs in blood was restored spontaneously with duration time of Sicca syndrome. We also examined the immunohistochemical staining of salivary glands of SS patients with monoclonal antibodies against fascin, CD11c and human leucocyte antigen DR (HLA-DR). Fascin(+) or CD11c(+)/HLA-DR+ mononuclear cells were present in the salivary glands of secondary SS patients, as in primary SS. However, fascin+ mononuclear cells were barely detected in the salivary glands of a chronic phase of SS patients. We also found a negative correlation between the frequency of blood myeloid DCs and salivary gland-infiltrating DCs in secondary SS patients, as well as primary SS. Our results suggest that the reduction of blood myeloid DCs and preferential trafficking of myeloid DCs into salivary glands is a common event in the early stage of SS. Myeloid DCs may play essential roles in the pathogenesis of Sicca syndrome of SS by initiating T helper cell immune responses.

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