ROLES OF SALIVARY GLAND CELLS AS ANTIGEN PRESENTING CELLS IN PATHOGENESIS OF SJOGRENS SYNDROME

本实验以自身免疫模型小鼠MRL/lpr和对照小鼠MRU+、MRL/+小鼠为研究对象，采用免疫组化方法，研究了唾液腺细胞作为抗原提呈细胞在干燥综合征发病机制中的作用。Study.通过麻醉过量随后放血处死每种品系的5月龄小鼠。取出下颌下腺，固定在10%缓冲福尔马林中，并包埋在石蜡中。石蜡包埋的组织切片（3μm）针对共刺激因子进行免疫染色，即。用链霉亲和素-生物素法检测了与自身反应性T细胞活化相关的CD 80、CD 8 G、4-1BB配体、OX 40配体、GITR配体。此外，Foxp 3，这是一个调节性T细胞标志物和转录因子，免疫组织化学定位进行了探索。MRL/lpr小鼠的下颌下腺标本显示导管细胞强烈表达这四种顺式刺激因子。然而，这些配体在MRL/+小鼠中的免疫定位是弱的，不令人信服的。此外，我们发现浸润性炎性细胞在所有四种共刺激因子均定位的下颌下腺标本中广泛扩增。已经阐明，一些共刺激因子可增强它们的功能，例如CD 80和OX 40配体，4-1BB配体和CD 80或CD 86，4-1BB和OX 40，以及CD 28和GYM。因此，四种共刺激因子的协同作用可能导致MRL/lpr小鼠自身免疫性涎腺炎中炎性细胞的强烈浸润，综合我们的研究表明，通过上调这五种共刺激因子的表达，作为抗原呈递细胞发挥关键作用的唾液腺导管细胞与MRL/lpr小鼠Sjogren综合征样涎腺炎的发生有关。

We examined immunohistochemically roles of salivary gland cells as antigen presenting cells in pathogenesis of Sjogren's syndrome using autoimmune model mouse, MRL/lpr mice, and control mice, MRU+ mice, MRL/+ mice, in our present. Study. 5-month-old mice of each strain were sacrificed by anesthesia overdose followed by exsanguinations. Submandibular glands were removed fixed in 10% buffered formalin, and embedded in paraffin. Paraffin-embedded tissue sections (3μm) were immunostained against costimulatory factors, ie. CD80, CD8G, 4-1BB ligand, OX40 ligand, GITR ligand, which are related to autoreactive T cells activation provoking autoimmune responses, using streptoavidin- biotin method. Additionally, immunohistochemical localization of Foxp3, which is one of regulatory T cell markers and a transcription factor, was explored. The submandibular gland specimens of MRL/lpr mice showed intense expression of these four cistimulatory factors in ductal cells. However, the immunolocalizations of these ligands in MRL/+ mice were weak and not convincing.Furthermore, we showed that infiltrating inflammatory cells were expanding extensively in submandibular gland specimens where all four costimulatory factors were localized. It has been clarified that some costimulatory factors reciprocally potentiate their functions, for example CD80 and OX40 ligand, 4-1BB ligand and CD80 or CD86, 4-1BB and OX40, and CD28 and GYM. Therefore, the synergy of four costimulatory factors possibly contributed to intensive inflammatory cell infiltration in autoimmune sialoadenitis of MRL/lpr mice.Taken together our present study indicates that salivary gland ductal cells that playa pivotal role as antigen presenting cells through upregulated expression of these 5 costimulatory factors has the association with the development of Sjogren's syndrome- like sialadenitis in MRL/lpr mice.