Presence of B7-2+ dendritic cells and expression of Th1 cytokines in the early development of sialodacryoadenitis in the IQI/Jic mouse model of primary Sjogren's syndrome

Presence of B7-2+ dendritic cells and expression of Th1 cytokines in the early development of sialodacryoadenitis in the IQI/Jic mouse model of primary Sjogren's syndrome
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DOI:
10.1080/0891693031000141077
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发表时间:
2003-07-01
期刊:
影响因子:
3.5
通讯作者:
Takiguchi, M
Takiguchi, M
中科院分区:
医学4区
文献类型:
--
作者:
Konno, A;Takada, K;Takiguchi, M

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在原发性干燥综合征的IQI/Jic小鼠模型中研究了可引发自身免疫性涎腺泪腺炎的浸润性淋巴细胞、专职抗原呈递细胞(APC)和Th 1/Th 2细胞因子的亚群。尽管淋巴细胞浸润首先见于8周龄时雌性的下颌下腺(SMG)和雄性的泪腺(LGs),4周时,CD 11 c(+)、B7-2(+)树突状细胞(DCs)已定位于这些组织中。8周时,浸润的淋巴细胞由几乎相等数量的B细胞和CD 4(+)T细胞组成。在炎症灶中,MHC Ⅱ类分子、CD 11 c(+)、B7-2(+)DCs形成网状结构。病变中的导管细胞显示MHC II类和ALCAM(共刺激粘附分子)的免疫反应性。RT-PCR检测到IL-12和IFN-γ在8-12周雌性SMG和雄性LGs中的表达,提示聚集的DC可能在淋巴结炎的发生中起重要作用,并进一步提示DC和上皮细胞可能参与了CD 4(+)T细胞的活化。Th 1细胞因子可能介导了早期病变中APC和CD 4(+)T细胞之间的功能性相互作用。
Subpopulations of infiltrating lymphocytes, professional antigen-presenting cells (APCs), and Th1/Th2 cytokines that could initiate an autoimmune sialodacryoadenitis were studied in the IQI/Jic mouse model of primary Sjogren's syndrome.Although lymphocytic infiltrations were first seen in submandibular glands (SMGs) of females and in lacrimal glands (LGs) of males at 8 weeks of age, clusters of MHC class II+ , CD11c(+) , B7-2(+) dendritic cells (DCs) were already localized in these tissues at 4 weeks. At 8 weeks, the infiltrating lymphocytes consisted of almost equal numbers of B cells and CD4(+) T cells. In the inflammatory foci, MHC class II+ , CD11c(+) , B7-2(+) DCs formed network-like structures. Duct cells in the lesions showed immunoreactivities for MHC class II and ALCAM (a costimulatory adhesion molecule). IL-12 and IFN-gamma transcripts were detected by RT-PCR in SMGs of females and in LGs of males at 8-12 weeks.These results suggest that the clustered DCs might play an important role in the initiation of the adenitis, and further suggest that the DCs and epithelial cells may participate in the activation of CD4(+) T cells. It is also likely that Th1 cytokines mediate the functional interactions between the APCs and CD4(+) T cells in the early lesions.