麻省理工学院科赫综合癌症研究所的研究人员已发现一个基因，它控制的过程能让抗体获得对抗逆转录病毒的能力。爱德华布朗指出，TLR7基因允许抗体产生B细胞以识别逆转录病毒，并促进生发中心反应，抗体通过这一过程能增强杀伤力。该研究结果发表在10月6日的《PLoS Pathogens》期刊上。
TLR7基因能调控抗体对逆转录病毒的应答
TLR7基因隶属于一类原始基因家族，它们的祖先序列在昆虫和蠕虫中被发现，然而，研究表明免疫系统挑选这类基因用于抗体合成的新目的。
抗体是我们机体对抗病毒疾病的一个关键成分，但对于一些病毒（如艾滋病毒），这种免疫应答严重地出现“故障”。感染艾滋病毒的病人会合成大量的无用抗体，这些抗体不具有杀伤艾滋病毒的能力。艾滋病毒感染期间为什么会出现这样情况？以及如何解决这个问题是艾滋病研究人员面临的最大挑战之一。
抗体会在生发中心反应中发生变异，经过筛选后功能最强大的抗体会成为“主宰”。布朗博士称，TLR7基因是研究中发现的一个重要基因，可特定地提高抗体应答水平。艾滋病患者体内这一过程的增强可以加快高亲和性、广谱性的中和抗体的形成。(生物探索译 Pobee)
相关英文论文摘要
Toll-like Receptor 7 Controls the Anti-Retroviral Germinal Center Response
The development of vaccines that can enhance immunity to viral pathogens is an important goal. However, the innate molecular pathways that regulate the strength and quality of the immune response remain largely uncharacterized. To define the role of Toll-like receptor (TLR) signaling in control of a model retroviral pathogen, Friend virus (FV), I generated mice in which the TLR signaling adapter Myd88 was selectively deleted in dendritic cell (DC) or in B cell lineages. Deletion of Myd88 in DCs had little effect on immune control of FV, while B cell specific deletion of Myd88 caused a dramatic increase in viral infectious centers and a significantly reduced antibody response, indicating that B cell-intrinsic TLR signaling plays a crucial role, while TLR signaling in DCs is less important. I then identified the single-stranded RNA sensing protein TLR7 as being required for antibody-mediated control of FV by analyzing mice deficient in TLR7. Remarkably, B cells in infected TLR7-deficient mice upregulated CD69 and CD86 early in infection, but failed to develop into germinal center B cells. CD4 T cell responses were also attenuated in the absence of TLR7, but CD8 responses were TLR7 independent, suggesting the existence of additional pathways for detection of retroviral particles. Together these results demonstrate that the vertebrate immune system detects retroviruses in vivo via TLR7 and that this pathway regulates a key checkpoint controlling development of germinal center B cells.
英文论文链接：https://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1002293
