本文選題：銀屑病 + T淋巴細胞　； 參考：《山東大學(xué)》2010年碩士論文

【摘要】： 研究背景銀屑病是一種常見的慢性炎癥性皮膚病,以角質(zhì)形成細胞異常增殖分化、真皮淺層炎細胞浸潤和血管增生擴張為基本病理特點。目前主要在免疫紊亂、表皮角質(zhì)形成細胞異常增殖和微血管增生異常等方面研究其發(fā)病機制,較一致的觀點認為銀屑病是一種多基因遺傳背景下的免疫介導(dǎo)的炎癥性皮膚病,免疫紊亂與銀屑病發(fā)生、發(fā)展及反復(fù)發(fā)作密切相關(guān)。皮損中的T淋巴細胞異�；罨倾y屑病病發(fā)生的關(guān)鍵,同時有樹突細胞、角質(zhì)形成細胞等多種免疫細胞及細胞因子的參與,共同構(gòu)成銀屑病的免疫發(fā)病過程。 樹突細胞具有激活靜止T淋巴細胞必需的所有特性,未成熟樹突細胞具有較強的攝取和加工抗原的功能,成熟的樹突細胞具有較強的遞呈抗原功能。樹突細胞與T淋巴細胞在銀屑病免疫機制中的關(guān)系日益受到研究者們的重視。樹突細胞的成熟標志DC-LAMP (DC-lysosomal-associated membrane protein,即CD208),是溶酶體相關(guān)膜蛋白(LAMP)家族的成員之一,其功能與樹突細胞內(nèi)MHC抗原復(fù)合物的加工和胞內(nèi)運輸過程有關(guān)。DC-SIGN (dendritic-cell specific ICAM-3 grabbing non-integrin,即CD209),是新發(fā)現(xiàn)的一種特異性表達在樹突細胞上的C-型凝集素,調(diào)節(jié)樹突細胞的多種免疫功能,在激活T淋巴細胞方面具有重要作用。DC-LAMP和DC-SIGN是調(diào)節(jié)樹突細胞與T淋巴細胞相互作用的兩個關(guān)鍵因子。 研究目的檢測DC-LAMP與DC-SIGN在尋常型銀屑病皮損組織中的表達,觀察其在尋常型銀屑病皮損組織與正常組織中表達水平的差異及相關(guān)性,探討DC-LAMP與DC-SIGN在銀屑病發(fā)病機制中的作用。 研究方法利用RT-PCR法和免疫組化法檢測33例尋常型銀屑病皮損組織和11例正常皮膚組織石蠟包埋組織標本中DC-LAMP、DC-SIGN的表達與定位。采用圖像分析技術(shù)定量分析尋常型銀屑病組織皮損與正常組織中DC-LAMP與DC-SIGN的表達差異,并進行相關(guān)性分析。 結(jié)果PCR結(jié)果顯示銀屑病組和正常組皮膚均擴增出符合要求的目的片段,銀屑病組DC-LAMP、DC-SIGN的基因表達水平均高于正常皮膚組。尋常型銀屑病皮損處DC-LAMP的陽性表達位于角質(zhì)形成細胞的基底層、棘層和真皮樹突細胞的胞漿中；DC-SIGN的陽性表達位于基底層、棘細胞層角質(zhì)形成細胞和真皮樹突細胞的胞漿、胞核中。DC-LAMP及DC-SIGN在尋常型銀屑病皮損組織中的表達明顯高于正常對照組,其差異具有統(tǒng)計學(xué)意義(P0.01)；DC-LAMP與DC-SIGN在尋常型銀屑病皮損組織中的表達呈正相關(guān)(P0.05,r=0.368)。 結(jié)論①DC-LAMP表達在尋常型銀屑病皮損內(nèi)表皮角質(zhì)形成細胞、真皮淺層樹突細胞的胞漿中,其基因轉(zhuǎn)錄水平和蛋白表達水平均明顯高于正常皮膚。②DC-SIGN表達在尋常型銀屑病皮損內(nèi)表皮角質(zhì)形成細胞、真皮淺層樹突細胞的胞漿和胞核中,其基因轉(zhuǎn)錄水平和蛋白表達水平均明顯高于正常皮膚。③DC-LAMP與DC-SIGN在銀屑病皮損的高表達呈正相關(guān),提示DC-LAMP和DC-SIGNP可能具有協(xié)同刺激T淋巴細胞活化的作用。④銀屑病角質(zhì)形成細胞表達DC-LAMP、DC-SIGN,參與皮損內(nèi)T淋巴細胞繼續(xù)活化。
[Abstract]:Background psoriasis is a common chronic inflammatory dermatosis. It is characterized by abnormal proliferation and differentiation of keratinocytes, infiltration of superficial dermatitis cells and proliferation of vascular proliferation. The pathogenesis is mainly in the aspects of immune disorder, abnormal proliferation of epidermal keratinocytes and abnormal blood Guan Zengsheng. The point of view is that psoriasis is an immune mediated inflammatory dermatosis in the genetic background of multiple genes. The immune disorder is closely related to the occurrence of psoriasis, development and recurrent attacks. The abnormal activation of T lymphocytes in the skin is the key to the occurrence of psoriasis, and there are many immune cells and fine cells, such as dendritic cells, keratinocytes, and so on. The participation of cytokines contributes to the pathogenesis of psoriasis.
Dendritic cells have all the necessary characteristics to activate static T lymphocytes. Immature dendritic cells have strong ability to absorb and process antigens. Mature dendritic cells have strong antigen presenting function. The relationship between dendritic cells and T lymphocytes in the immune mechanism of psoriasis is being paid more and more attention by researchers. The maturation marker, DC-LAMP (DC-lysosomal-associated membrane protein, CD208), is one of the members of the lysosomal related membrane protein (LAMP) family. Its function is related to the processing of the MHC antigen complex in the dendritic cells and the intracellular transport process associated with.DC-SIGN (dendritic-cell specific ICAM-3 grabbing), which is a new discovery. A type of C- agglutinin specifically expressed on dendritic cells, regulating various immune functions of dendritic cells and playing an important role in activating T lymphocytes,.DC-LAMP and DC-SIGN are two key factors regulating the interaction of dendritic cells and T lymphocytes.
Objective to detect the expression of DC-LAMP and DC-SIGN in the skin lesions of psoriasis vulgaris, to observe the difference and correlation between the expression level of psoriasis vulgaris and normal tissues, and to explore the role of DC-LAMP and DC-SIGN in the pathogenesis of psoriasis.
The expression and localization of DC-LAMP and DC-SIGN in 33 cases of psoriasis vulgaris skin tissue and 11 normal skin tissue specimens were detected by RT-PCR and immunohistochemistry. The difference between the tissue skin lesions of psoriasis vulgaris and the expression of DC-LAMP and DC-SIGN in normal fabric was analyzed by image analysis. Correlation analysis.
Results the results of PCR showed that both the psoriasis group and the normal group amplified the desired target segments. The expression level of DC-LAMP and DC-SIGN in psoriasis group was higher than that in the normal skin group. The positive expression of DC-LAMP in psoriasis vulgaris lesions was located in the basal layer of keratinocytes, the spinous and dermis dendritic cells in the cytoplasm; DC-SIGN The positive expression was located in the basal layer, the acanthocyte layer keratinocyte and the cytoplasm of the dermis dendritic cells. The expression of.DC-LAMP and DC-SIGN in the skin lesions of psoriasis vulgaris was significantly higher than that of the normal control group, and the difference was statistically significant (P0.01). The expression of DC-LAMP and DC-SIGN in the skin lesions of psoriasis vulgaris Positive correlation (P0.05, r=0.368).
Conclusion (1) the expression of DC-LAMP in the epidermis of epidermal keratinocytes in psoriasis vulgaris and in the cytoplasm of the superficial dendritic cells of the dermis is significantly higher than that of the normal skin. (2) the expression of DC-SIGN in the epidermis of the epidermis and the nucleus of the superficial dendrite cells in the skin of psoriasis vulgaris. The gene transcription level and protein expression level were significantly higher than normal skin. (3) DC-LAMP and DC-SIGN were positively correlated with the high expression of psoriatic skin lesions, suggesting that DC-LAMP and DC-SIGNP may have synergistic stimulation of T lymphocyte activation. 4. Keratinocytes of psoriasis express DC-LAMP, DC-SIGN, and participate in T lymphocytes in skin lesions. Continued activation.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2010
【分類號】：R758.63

【參考文獻】

相關(guān)期刊論文 前10條

1 李丹,匡凱英;DC-SIGN結(jié)構(gòu)和功能的研究進展[J];國外醫(yī)學(xué)(免疫學(xué)分冊);2002年04期

2 胡佳,張美華;樹突狀細胞在炎癥性皮膚病中的作用[J];臨床皮膚科雜志;2005年11期

3 何玉清;銀屑病免疫病理學(xué)研究進展[J];嶺南皮膚性病科雜志;2002年04期

4 孫宏偉;杜華;楊桂蘭;;銀屑病病因與發(fā)病機制的研究進展[J];中國麻風(fēng)皮膚病雜志;2008年01期

5 李俊琴;張開明;;銀屑病T細胞活化的再認識[J];中國麻風(fēng)皮膚病雜志;2008年08期

6 劉巍,周同,史浩,孫桂芝,陳楠,張冬青;細胞粘附與樹突狀細胞遷移機制[J];生命科學(xué);2002年06期

7 李軍,馮志華;DC-SIGN與微生物感染研究進展[J];世界華人消化雜志;2005年05期

8 張峻嶺,陳學(xué)榮,殷金珠;β-溶血型鏈球菌與角質(zhì)形成細胞增殖和凋亡研究[J];中國皮膚性病學(xué)雜志;2000年05期

9 李新華,康玉英,張開明;SAg作用的銀屑病T細胞對表皮c-myc bcl-2及P53蛋白的影響[J];中國皮膚性病學(xué)雜志;2004年11期

10 李萍,夏立新,高奎斌,張亞芹,王雅坤,陳洪鐸;結(jié)合珠蛋白在銀屑病皮損及皮損周邊外觀正常皮膚中的表達[J];中華皮膚科雜志;2004年03期

，

本文編號：2103925