| 1 | Repression of the Auxin Response Pathway Increases Arabidopsis Susceptibility to Necrotrophic Fungi显示文摘在植物,到 necrotrophic 病原体的抵抗取决于在不同荷尔蒙系统之间的相互影响,例如水杨酸调整的那些酸(SA ) , jasmonic 酸(JA ) ,乙烯,和 abscisic 酸。由 SA 小径发信号的植物生长素的压抑最近被显示贡献抗菌剂抵抗。这里,我们表明表明在刺激植物生长素的 SCF (Skp1CullinF 盒子) ubiquitination 小径展览有缺点的异种 axr1, axr2,和 axr6 的那 Arabidopsis 植物生长素增加的危险性到 necrotrophic 真菌 Plectosphaerella cucumerina 和 Botrytis cinerea。另外,被 SCF-ubiquitin/proteasome 机械通常为移动指向的植物生长素 transcriptional 抑压者 AXR3 的稳定发生在 P 之上。cucumerina 感染。植物生长素运输或 proteasome 功能的药理学抑制各作为在非对待的植物生长素反应异种损害野类型的植物的 necrotroph 抵抗到类似的程度。这些结果建议植物生长素发信号为到 necrotrophic 真菌 P 的抵抗是重要的。cucumerina 和 B。cinerea。SGT1b (编码 HSP90/HSC70 合作女伴的二 Arabidopsis SGT1 基因之一) 在某些抵抗(R) 基因调节到 biotrophic 病原体的植物生长素和 JA 回答和抵抗支持 SCF E3-ubiquitin ligase 建筑群的功能。我们发现 sgt1b 异种对 P 同样抵抗。是的 cucumerina 野类型的植物。相反地, auxin/SCF 发信号异种在到 obligate biotrophic oomycete 的被触发 RPP4 的抵抗是不妥协的, Hyaloperonospora parasitica。因此,在到 oomycetes 的 R 调节基因的抵抗的 SGT1b 的占优势的行动看起来在除帮助 SCF E3-ubiquitin ligases 以外的一个地点。然而, sgt1b axr1 的基因添加在到 H 的危险性的两倍异种。一旦 plantpathogen 相容性被建立, parasitica 建议调停 SCF 的 ubiquitination 贡献限制 biotrophic 病原体殖民。 | Francisco Llorente Paul M usksktt Andrea Sanchez-Vallet Gemma Lopez Brisa Ramos Clara Sanchez-Rodriguez Lucia Jorda Jane Parker Antonio Molina | 2008 | Molecular Plant2008，1，3： | 8 |
| 3 | In vitro intracellular IFNγ, IL-17 and IL-10 producing T cells correlates with the occurrence of post-transplant opportunistic infection in liver and kidney recipients显示文摘AIM To validate intracellular cytokine production functional assay as means of cell-mediated immunity monitoring of post-transplant patients with opportunistic infection(OI).METHODS Intracellular cytokine-producing CD4^+ and CD8^+ T-cell monitoring was carried out in 30 liver transplant(LTr) and 31 kidney transplant(KTr) recipients from 2010 to 2012. Patients were assessed in our Department of Immunology at the Clinical University ‘Hospital Virgen de la Arrixaca-IMIB' in Murcia, Spain for one year following transplantation. FACS Canto Ⅱ flow cytometer was employed to quantify the intracellular production of IL-17, IFNγ and IL-10 cytokines on stimulated CD4^+CD69^+ and CD8^+CD69^+ T cells and BD FACS DIVA v.6 software was used to analysed the data. Statistical analysis was carried out using SPSS 22.0.RESULTS LTr with OI had significantly lower % of CD8^+CD69^+IFNγ^+T cells at 60(7.95 ± 0.77 vs 26.25 ± 2.09, P < 0.001), 90(7.47 ± 1.05 vs 30.34 ± 3.52, P < 0.001) and 180(15.31 ± 3.24 vs 24.59 ± 3.28, P = 0.01) d posttransplantation. Higher % of CD4^+CD69^+IL-10^+ as well as CD4^+CD69^+IL-17^+ T cells were yet reported at 30(14.06 ± 1.65 vs 6.09 ± 0.53, P = 0.0007 and 4.23 ± 0.56 vs 0.81 ± 0.14, P = 0.005; respectively), 60(11.46 ± 1.42 vs 4.54 ± 0.91, P = 0.001 and 4.21 ± 0.59 vs 1.43 ± 0.42, P = 0.03; respectively) and 90 d(16.85 ± 1.60 vs 4.07 ± 0.63, P < 0.001 and 3.97 ± 0.43 vs 0.96 ± 0.17, P = 0.001). Yet, KTr with OI had significantly lower percentage of CD4^+CD69^+IFNγ^+ at 30(11.80 ± 1.59 vs 20.64 ± 3.26, P = 0.035), 60(11.19 ± 1.35 vs 15.85 ± 1.58, P = 0.02), 90(11.37 ± 1.42 vs 22.99 ± 4.12, P = 0.028) and 180(13.63 ± 2.21 vs 21.93 ± 3.88, P = 0.008) d post-transplantation as opposed to CD4^+CD69^+IL-10^+ and CD8^+CD69^+IL-10^+ T cells which percentages were higher at 30(25.21 ± 2.74 vs 8.54 ± 1.64, P < 0.001 and 22.37 ± 1.35 vs 17.18 ± 3.54, P = 0.032; respectively), 90(16.85 ± 1.60 vs 4.07 ± 0.63, P < 0.001 and 23.06 ± 2.89 vs 10.19 ± 1.98, P = 0.002) and 180(21.81 ± 1.72 vs 6.07 ± 0.98, P < 0.001 and 19.68 ± 2.27 vs 10.59 ± 3.17, P = 0.016) d posttransplantation. The au ROC curve model determined the most accurate cut-off values to stratify LTr and KTr at high risk of OI and Cox Regression model confirmed these biomarkers as the most significant risk factors to opportunistic infection.CONCLUSION Post-transplant percentages of T-cell subsets differed significantly amongst infected-and non-infected-LTr and-KTr and yet this imbalance was found to contribute towards a worst clinical outcome. | Francisco Boix Santiago Llorente Jorge Eguía Gema Gonzalez-Martinez Rafael Alfaro Jose A Galián Jose A Campillo María Rosa Moya-Quiles Alfredo Minguela Jose A Pons Manuel Muro | 2018 | World Journal of Transplantation2018，8，1： | 0 |
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