Valencia Pacheco Guillermo J, Pinzón Herrera Francisc, Cruz López Juan J, Vera Gamboa Ligia Del Carmen, Pavía Ruiz Norma, Santos Rivero Adrián, Sánchez Lugo Saulo, Puerto Fernando
Universidad Autónoma de Yucatán. Mérida, Yucatán, Méx. E-mail:
Centro Ambulatorio para la Prevención y Atención del SIDA y otras ITS (CAPASITS). Servicios de Salud de Yucatán. Mérida, Yucatán, Méx. E-mail:
Colomb Med (Cali). 2013 Jun 30;44(2):92-9. eCollection 2013 Apr.
TLR´s play a role in host defense in HIV infection recognizing the viral DNA or RNA. Their activation induces a signaling pathway that includes the proteins MyD88, IRAK4, TRAF6 and the transcription factor NF-kBp65.
To determine the expression of TLR7, TLR8 and TLR9, and activation of its signaling pathway in monocytes from patients infected with HIV. Methods. Expression of TLR7, TLR8 and TLR9 was determined in monocytes from HIV-infected patients (n= 13) and control subjects (n= 13), which were activated with specific ligands. The expression of MyD88 and NF-kBp65 were determined by flow cytometry; IRAK4 and TRAF6 were studied by immunoblotting.
No statistical difference was found in the expression of TLR7, 8 and 9 in monocytes from patients compared to controls, but we observed the non-significant increased expression of TLR9 in patients. The activation showed no significant difference in the expression of MyD88 and NF-kBp65 in patients when compared to controls, but were decreased in stimulated cells over non-stimulated cells. IRAK4 and TRAF6 were not detected.
No statistical difference was observed in the expression of intracellular TLRs, MyD88 and NFkBp65 in monocytes from patients compared to controls. This was probably due to effective antiretroviral therapy being received at the time of study entry. Additional studies are needed under controlled conditions that include infected patients with and without ARVT, responders and non-responders, and work with different cell populations.
Toll样受体(TLR)在识别病毒DNA或RNA的HIV感染宿主防御中发挥作用。它们的激活诱导了一条信号通路,该通路包括MyD88、IRAK4、TRAF6蛋白和转录因子NF-κBp65。
确定HIV感染患者单核细胞中TLR7、TLR8和TLR9的表达及其信号通路的激活情况。方法:测定HIV感染患者(n = 13)和对照受试者(n = 13)单核细胞中TLR7、TLR8和TLR9的表达,并用特异性配体激活这些细胞。通过流式细胞术测定MyD88和NF-κBp65的表达;通过免疫印迹法研究IRAK4和TRAF6。
与对照组相比,患者单核细胞中TLR7、8和9的表达无统计学差异,但我们观察到患者中TLR9表达有非显著性增加。与对照组相比,患者中MyD88和NF-κBp65的激活表达无显著差异,但与未刺激细胞相比,刺激细胞中的表达降低。未检测到IRAK4和TRAF6。
与对照组相比,患者单核细胞中细胞内TLR、MyD88和NF-κBp65的表达未观察到统计学差异。这可能是由于研究入组时接受了有效的抗逆转录病毒治疗。需要在包括接受和未接受抗逆转录病毒治疗的感染患者、反应者和无反应者以及不同细胞群体的受控条件下进行更多研究。