Poudrier Johanne, Soulas Caroline, Chagnon-Choquet Josiane, Burdo Tricia, Autissier Patrick, Oskar Kathryn, Williams Kenneth C, Roger Michel
Laboratoire d'immunogénétique, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, Canada; Département de Microbiologie, Infectiologie et Immunologie de l'Université de Montréal, Montréal, Canada.
Boston College, Boston, MA, United States of America.
PLoS One. 2015 Jun 24;10(6):e0131513. doi: 10.1371/journal.pone.0131513. eCollection 2015.
Dendritic cells (DCs) modulate B-cell survival and differentiation, mainly through production of growth factors such as B lymphocyte stimulator (BLyS/BAFF). In recent longitudinal studies involving HIV-1-infected individuals with different rates of disease progression, we have shown that DCs were altered in number and phenotype in the context of HIV-1 disease progression and B-cell dysregulations were associated with increased BLyS/BAFF expression in plasma and by blood myeloid DCs (mDCs) in rapid and classic progressors but not in HIV-1-elite controllers (EC). Suggesting that the extent to which HIV-1 disease progression is controlled may be linked to BLyS/BAFF expression status and the capacity to orchestrate B-cell responses. Herein, longitudinal analyses of simian immunodeficiency virus (SIV)-infected rhesus macaques also revealed increased expression of BLyS/BAFF by blood mDCs as soon as day 8 and throughout infection. Strikingly, granulocytes presented the highest BLyS/BAFF expression profile in the blood of SIV-infected macaques. BLyS/BAFF levels were also increased in plasma and correlated with viral loads. Consequently, these SIV-infected animals had plasma hyperglobulinemia and reduced blood B-cell numbers with altered population frequencies. These data underscore that BLyS/BAFF is associated with immune dysregulation in SIV-infected rhesus macaques and suggest that BLyS/BAFF is a key regulator of immune activation that is highly conserved among primates. These findings emphasize the potential importance of this SIV-infected primate model to test whether blocking excess BLyS/BAFF has an effect on the overall inflammatory burden and immune restoration.
树突状细胞(DCs)主要通过产生诸如B淋巴细胞刺激因子(BLyS/BAFF)等生长因子来调节B细胞的存活和分化。在最近涉及不同疾病进展速率的HIV-1感染个体的纵向研究中,我们发现,在HIV-1疾病进展过程中,DCs的数量和表型发生了改变,并且B细胞失调与快速进展者和典型进展者血浆及血液髓样DCs(mDCs)中BLyS/BAFF表达增加有关,但在HIV-1精英控制者(EC)中并非如此。这表明HIV-1疾病进展的控制程度可能与BLyS/BAFF表达状态以及协调B细胞反应的能力有关。在此,对感染猴免疫缺陷病毒(SIV)的恒河猴的纵向分析还显示,早在感染第8天及整个感染过程中,血液mDCs中BLyS/BAFF的表达就增加了。令人惊讶的是,粒细胞在感染SIV的猕猴血液中呈现出最高的BLyS/BAFF表达谱。血浆中BLyS/BAFF水平也升高,且与病毒载量相关。因此,这些感染SIV的动物出现血浆球蛋白血症,血液B细胞数量减少,群体频率改变。这些数据强调,BLyS/BAFF与感染SIV的恒河猴的免疫失调有关,并表明BLyS/BAFF是免疫激活的关键调节因子,在灵长类动物中高度保守。这些发现强调了这种感染SIV的灵长类动物模型对于测试阻断过量BLyS/BAFF是否对整体炎症负担和免疫恢复有影响的潜在重要性。