目的 探討主要組織相容性復合體(MHC)Ⅱ類基因的反式轉(zhuǎn)錄因子（CⅡTA）在多器官功能障礙綜合征（MODS）中對MHCⅡ類基因的調(diào)控機理。方法 18只雄性家豬隨機分為實驗組（n=9）和對照組(n=9)。實驗組給予失血性休克、再灌注損傷、內(nèi)毒素血癥等復合干擾因素，建立二次打擊豬MODS模型； 對照組僅進行麻醉和動靜脈插管。7 d后處死存活動物。切取實驗組造模成功動物和對照組動物的脾臟組織，用Trizol法提取總RNA。設計CⅡTA和豬MHCⅡ類基因(SLA-DQA)引物序列，逆轉(zhuǎn)錄構(gòu)建cDNA，行實時熒光定量PCR檢測。UVP計算機圖像分析系統(tǒng)繪出標準曲線并得出2組CⅡTA mRNA和SLA-DQA mRNA的拷貝數(shù)。以Pearson法分析MODS動物CⅡTA mRNA和SLA-DQA mRNA表達的相關性。結(jié)果 實驗組動物死亡7例，有8例發(fā)生MODS。對照組動物CⅡTA mRNA的拷貝數(shù)為（3.516±1.237）×103，實驗組MODS動物為（0.367±0.088）×103，差異有統(tǒng)計學意義（P=0.000）； 對照組SLA-DQA mRNA拷貝數(shù)為（5.330±3.053）×103，實驗組為（1.376±1.006）×103，差異亦有統(tǒng)計學意義(P=0.002)。MODS動物中CⅡTA mRNA和SLA-DQA mRNA的表達呈正相關(Pearson值為0.499，P=0.017)。結(jié)論 MODS模型復制滿意。MHCⅡ類基因在MODS中表達下降與CⅡTA的調(diào)控有關。
引用本文： 柴琛,薛左良,曹農(nóng),王斌生,李強. 反式轉(zhuǎn)錄因子在多器官功能障礙綜合征中對MHCⅡ類基因的調(diào)控. 中國普外基礎與臨床雜志, 2010, 17(11): 1190-1192. doi: 復制
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| 6. | Harton JA, Ting JP. Class Ⅱ transactivator: mastering the art of major histocompatibility complex expression [J]. Mol Cell Biol, 2000; 20(17): 6185-6194. |
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| 8. | Otten LA, Steimle V, Bontron S, et al. Quantitative control of MHC class Ⅱ expression by the transactivator CⅡTA [J]. Eur J Immunol, 1998; 28(2): 473-478. |
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| 10. | Kanazawa S, Okamoto T, Peterlin BM. Tat competes with CⅡTA for the binding to P-TEFb and blocks the expression of MHC class Ⅱ genes in HIV infection [J]. Immunity, 2000; 12(1): 61-70. |
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| 12. | 歐啟水, 林琪, 蘭斌， 等. CⅡTA基因修飾樹突狀細胞增強荷肝癌小鼠抗瘤效應 [J]. 細胞與分子免疫學雜志， 2005; 21(5): 580-582, 586. |
- 1. 柴琛， 方國恩， 沈賢， 等. 主要組織相容性復合體Ⅱ類基因在多器官功能障礙綜合征中的表達及意義 [J]. 中華創(chuàng)傷雜志， 2006; 22(11): 839-842.
- 2. Hu S, Sheng Z, Zhou B, et al. Study on delay two-phase multiple organ dysfunction syndrome [J]. Chin Med J (Engl), 1998; 111(2): 101-108.
- 3. Friese MA, Jones EY, Fugger L. MHC Ⅱ molecules in inflammatory diseases: interplay of qualities and quantities [J]. Trends Immunol, 2005; 26(11): 559-561.
- 4. Pachot A, Monneret G, Brion A, et al. Messenger RNA expression of major histocompatibility complex class Ⅱ genes in whole blood from septic shock patients [J]. Crit Care Med, 2005; 33(1): 31-38.
- 5. Steimle V, Otten LA, Zufferey M, et al. Complementation cloning of an MHC class Ⅱ transactivator mutated in hereditary MHC class Ⅱ deficiency (or bare lymphocyte syndrome) [J]. Cell, 1993; 75(1): 135-146.
- 6. Harton JA, Ting JP. Class Ⅱ transactivator: mastering the art of major histocompatibility complex expression [J]. Mol Cell Biol, 2000; 20(17): 6185-6194.
- 7. Steimle V, Siegrist CA, Mottet A, et al. Regulation of MHC class Ⅱ expression by interferon-gamma mediated by the transactivator gene CⅡTA [J]. Science, 1994; 265(5168): 106-109.
- 8. Otten LA, Steimle V, Bontron S, et al. Quantitative control of MHC class Ⅱ expression by the transactivator CⅡTA [J]. Eur J Immunol, 1998; 28(2): 473-478.
- 9. Peretti M, Villard J, Barras E, et al. Expression of the three human major histocompatibility complex class Ⅱ isotypes exhibits a differential dependence on the transcription factor RFXAP [J]. Mol Cell Biol, 2001; 21(17): 5699-5709.
- 10. Kanazawa S, Okamoto T, Peterlin BM. Tat competes with CⅡTA for the binding to P-TEFb and blocks the expression of MHC class Ⅱ genes in HIV infection [J]. Immunity, 2000; 12(1): 61-70.
- 11. Schooten E, Klous P, van den Elsen PJ, et al. Lack of MHC-Ⅱ expression in activated mouse T cells correlates with DNA methylation at the CⅡTA-PⅢ region [J]. Immunogenetics, 2005; 57(10): 795-799.
- 12. 歐啟水, 林琪, 蘭斌， 等. CⅡTA基因修飾樹突狀細胞增強荷肝癌小鼠抗瘤效應 [J]. 細胞與分子免疫學雜志， 2005; 21(5): 580-582, 586.