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首页> 外文期刊>International journal of infectious diseases : >CD4+CD25+CD127 regulatory cells play multiple roles in maintaining HIV-1 p24 production in patients on long-term treatment: HIV-1 p24-producing cells and suppression of anti-HIV immunity
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CD4+CD25+CD127 regulatory cells play multiple roles in maintaining HIV-1 p24 production in patients on long-term treatment: HIV-1 p24-producing cells and suppression of anti-HIV immunity

机译：CD4 + CD25 + CD127调节细胞在长期治疗的患者中维持HIV-1 p24产生多种作用：产生HIV-1 p24的细胞和抗HIV免疫抑制

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Background: A major question when attempting to eradicate and treat HIV-1 infection is how to reactivate latent proviruses. Stimulating HIV-1-specific cytolytic T lymphocytes (CTL) has been shown to facilitate the elimination of the latent viral reservoir after viral reactivation. Regulatory T (Treg) cells are known to be capable of lowering both HIV-specific immunoreactions and general immune activation during HIV-1 infection. It was hypothesized that the depletion of Treg cells could increase the HIV-1-specific cytolytic T lymphocyte response and reactivate HIV-1 p24 production. Methods: Treg cells were isolated by isolation kit according to the surface marker of Treg cells. Real-time PCR method was used to quantify HIV-1 DNA. P24 antigens in the cell culture supernatant was done by ELISA. Cells activation and HIV specific HIV-1 CD8+ T cells were analyses using a FACSCalibur flow cytometer and CELLQUEST software. Results: This study included both HIV-infected patients who were antiviral treatment-naive and patients with sustained viral responses to antiretroviral therapy (ART) for 1 or 5 years. It was found that the HIV-DNA levels in Treg cells were approximately 10-fold higher than those in non-Treg CD4+ cells and that the depletion of Treg cells could enhance the frequency of HIV-1-specific CTL and immune activation after 5 years of effective ART. Conclusions: CD4+CD25+CD127 regulatory cells play multiple roles in maintaining HIV-1 p24 production in long-term ART patients. Treg cells may be a target for eliminating the latent HIV reservoir after effective long-term ART.
机译：背景：尝试根除和治疗HIV-1感染时的主要问题是如何重新激活潜在的前病毒。已显示刺激HIV-1特异性溶细胞性T淋巴细胞（CTL）可以促进病毒重新激活后消除潜在的病毒库。已知调节性T（Treg）细胞能够降低HIV-1感染期间的HIV特异性免疫反应和一般的免疫激活。假设Treg细胞的耗竭可以增加HIV-1特异性溶细胞性T淋巴细胞反应并重新激活HIV-1 p24的产生。方法：根据Treg细胞的表面标记，用分离试剂盒分离Treg细胞。实时PCR方法用于定量HIV-1 DNA。细胞培养上清液中的P24抗原通过ELISA进行。使用FACSCalibur流式细胞仪和CELLQUEST软件分析细胞活化和HIV特异性HIV-1 CD8 + T细胞。结果：该研究既包括未接受过抗病毒治疗的HIV感染患者，也包括对抗逆转录病毒治疗（ART）持续病毒反应1或5年的患者。发现Treg细胞中的HIV-DNA水平比非Treg CD4 +细胞高约10倍，并且Treg细胞的耗竭可以提高HIV-1特异性CTL的频率和5年后的免疫激活有效的ART。结论：CD4 + CD25 + CD127调节细胞在长期ART患者中维持HIV-1 p24的产生中起多种作用。在有效的长期抗逆转录病毒治疗后，Treg细胞可能成为消除潜在HIV储备的靶标。

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