Amu Sylvie, Lavy-Shahaf Gitit, Cagigi Alberto, Hejdeman Bo, Nozza Silvia, Lopalco Lucia, Mehr Ramit, Chiodi Francesca
Retrovirology. 2014 Sep 11;11:76. doi: 10.1186/s12977-014-0076-x.
Aged individuals respond poorly to vaccination and have a higher risk of contracting infections in comparison to younger individuals; whether age impacts on the composition and function of B cell subpopulations relevant for immune responses is still controversial. It is also not known whether increased age during HIV-1 infection further synergizes with the virus to alter B cell subpopulations. In view of the increased number of HIV-1 infected patients living to high age as a result of anti-retroviral treatment this is an important issue to clarify.
In this work we evaluated the distribution of B cell subpopulations in young and aged healthy individuals and HIV-1 infected patients, treated and naïve to treatment. B cell populations were characterized for the expression of inhibitory molecules (PD-1 and FcRL4) and activation markers (CD25 and CD69); the capacity of B cells to respond to activation signals through up-regulation of IL-6 expression was also evaluated. Increased frequencies of activated and tissue-like memory B cells occurring during HIV-1 infection are corrected by prolonged ART therapy. Our findings also reveal that, in spite of prolonged treatment, resting memory B cells in both young and aged HIV-1 infected patients are reduced in number, and all memory B cell subsets show a low level of expression of the activation marker CD25.
The results of our study show that resting memory B cells in ART-treated young and aged HIV-1 infected patients are reduced in number and memory B cell subsets exhibit low expression of the activation marker CD25. Aging per se in the HIV-1 infected population does not worsen impairments initiated by HIV-1 in the memory B cell populations of young individuals.
与年轻个体相比,老年个体对疫苗接种反应不佳,感染风险更高;年龄是否会影响与免疫反应相关的B细胞亚群的组成和功能仍存在争议。此外,尚不清楚HIV-1感染期间年龄增长是否会与病毒进一步协同作用,改变B细胞亚群。鉴于抗逆转录病毒治疗使活到高龄的HIV-1感染患者数量增加,这是一个需要阐明的重要问题。
在这项研究中,我们评估了年轻和老年健康个体以及接受治疗和未接受治疗的HIV-1感染患者中B细胞亚群的分布。对B细胞群体进行了抑制分子(PD-1和FcRL4)和激活标志物(CD25和CD69)表达的表征;还评估了B细胞通过上调IL-6表达对激活信号作出反应的能力。HIV-1感染期间出现的活化和组织样记忆B细胞频率增加可通过延长抗逆转录病毒治疗得到纠正。我们的研究结果还表明,尽管进行了长期治疗,但年轻和老年HIV-1感染患者的静息记忆B细胞数量均减少,并且所有记忆B细胞亚群均显示激活标志物CD25的低表达水平。
我们的研究结果表明,接受抗逆转录病毒治疗的年轻和老年HIV-1感染患者的静息记忆B细胞数量减少,并且记忆B细胞亚群显示激活标志物CD25的低表达。在HIV-1感染人群中,衰老本身不会使年轻个体记忆B细胞群体中由HIV-1引发的损伤恶化。