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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >A T2 cytokine environment may not limit T1 responses in human immunodeficiency virus patients with a favourable response to antiretroviral therapy.
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A T2 cytokine environment may not limit T1 responses in human immunodeficiency virus patients with a favourable response to antiretroviral therapy.

机译：T2细胞因子环境可能不会限制人类免疫缺陷病毒患者对抗逆转录病毒疗法产生良好反应的T1反应。

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摘要

Low-level production of interferon-gamma (IFN-gamma) marks human immunodeficiency virus (HIV)-induced immunodeficiency and has been ascribed to a bias towards T2 cytokines. This was investigated in two cross-sectional studies of HIV patients who were immunodeficient when they began antiretroviral therapy (ART) and had stable increases in CD4 T-cell counts. Blood leucocytes were assessed unstimulated or after stimulation with cytomegalovirus (CMV), anti-CD3 or mitogen. IFN-gamma and interleukin (IL)-5 responses were initially assessed by enzyme-linked immunosorbent spot-forming cell assay (ELISPOT) and enzyme-linked immunosorbent assay (ELISA). We then adopted a sensitive reverse transcription-polymerase chain reaction (RT-PCR) system to assess IFN-gamma, IL-5, IL-4 and IL-4delta2 (an inhibitory splice variant of IL-4) mRNA. The results were correlated with putative serological markers of a T1 [lymphocyte activation gene-3 (LAG-3), CD26] or a T2 [CD30, immunoglobulin E (IgE)] cytokine environment. IL-5 production and IgE levels were elevated in patients. IgE levels did not correlate with IFN-gamma, but showed an inverse correlation with IL-5 released in culture (P = 0.05). The levels of IL-4, IFN-gamma, IL-5 and IL-4delta2 mRNA were correlated after anti-CD3 stimulation, where IL-5 was the best predictor of IFN-gamma mRNA (P = 0.006). Weak positive correlations were evident between CD30 and cytokine mRNA levels, whilst IgE correlated inversely with IL-4, IL-4delta2, IL-5 and IFN-gamma mRNA levels. These analyses provide no evidence for an inverse relationship between T1 and T2 cytokine responses in HIV patients, but suggest that the elevation of IgE marks low cytokine responses.
机译：干扰素-γ（IFN-γ）的少量生产标志着人类免疫缺陷病毒（HIV）诱导的免疫缺陷，并已归因于T2细胞因子的偏倚。在两项横断面研究中对HIV患者进行了调查，这些患者在开始抗逆转录病毒疗法（ART）时免疫缺陷，并且CD4 T细胞计数稳定增加。评估未刺激或用巨细胞病毒（CMV），抗CD3或促分裂原刺激后的血白细胞。最初通过酶联免疫吸附点形成细胞测定法（ELISPOT）和酶联免疫吸附测定（ELISA）评估IFN-γ和白介素（IL）-5应答。然后，我们采用了敏感的逆转录聚合酶链反应（RT-PCR）系统来评估IFN-γ，IL-5，IL-4和IL-4delta2（IL-4的抑制性剪接变体）mRNA。结果与T1 [淋巴细胞活化基因3（LAG-3），CD26]或T2 [CD30，免疫球蛋白E（IgE）]细胞因子环境的血清学标记有关。患者的IL-5产生和IgE水平升高。 IgE水平与IFN-γ不相关，但与培养物中释放的IL-5呈负相关（P = 0.05）。抗CD3刺激后，IL-4，IFN-γ，IL-5和IL-4delta2 mRNA的水平相关，其中IL-5是IFN-γmRNA的最佳预测因子（P = 0.006）。 CD30和细胞因子mRNA水平之间存在弱的正相关，而IgE与IL-4，IL-4delta2，IL-5和IFN-γmRNA水平呈负相关。这些分析没有提供证据证明HIV患者中T1和T2细胞因子反应呈反比关系，但表明IgE升高标志着低细胞因子反应。

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