McFarland Hugh I, Berkson Julia D, Lee Jay P, Elkahloun Abdel G, Mason Karen P, Rosenberg Amy S
Division of Research and Review 3, Office of Biotechnology Products, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, 10903 New Hampshire Ave., Silver Spring, MD 20993, USA.
Division of Research and Review 3, Office of Biotechnology Products, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, 10903 New Hampshire Ave., Silver Spring, MD 20993, USA; George Washington School of Medicine and Health Sciences, Ross Hall, 2300 Eye St. NW, Washington, DC 20037, USA.
Vaccine. 2015 Jul 31;33(32):3865-72. doi: 10.1016/j.vaccine.2015.06.070. Epub 2015 Jun 26.
Sublethal γ irradiation eliminates CD8+ T cell mediated memory responses. In this work, we explored how these memory responses could be rescued in the aftermath of such exposure. We utilized two models of CD8+ T cell mediated immunity: a mouse model of Listeria monocytogenes (LM) infection in which CD8+ T cells specific for LM expressed antigens (Listeriolysin O, LLO) can be tracked, and a murine skin graft model in which CD8+ T cells mediate rejection across a MHC class I (D(d)) disparity. In the LM immunized mice, LL0 specific CD8+ T memory cells were lost on irradiation, preserved with rapid revaccination with an attenuated strain 1-3 days post-irradiation (PI), and these mice survived a subsequent wild type LM challenge. A genetic "signature of rescue" identified a group of immune-associated mRNA maintained or upregulated following irradiation and rescue. A number of these factors, including IL-36γ, dectin-2 (Clec4n), and mir101c are upregulated rapidly after exposure of mice to sublethal γ radiation alone and are sustained by early, but not later rescue. Such factors will be evaluated as potential therapeutics to replace individual vaccines for global rescue of CD8+ T memory cell responses following sublethal γ irradiation. The skin allograft model mirrored that of the LM model in that the accelerated D(d) skin allograft rejection response was lost in mice exposed to sublethal γ radiation, but infusion of allogeneic D(d) expressing bone marrow cells 1-4 days PI preserved the CD8+ T memory mediated accelerated rejection response, further suggesting that innate immune responses may not always be essential to rescue of CD8+ memory T cells following γ irradiation.
亚致死剂量的γ射线照射会消除CD8 + T细胞介导的记忆反应。在这项研究中,我们探索了在这种照射后如何挽救这些记忆反应。我们使用了两种CD8 + T细胞介导免疫的模型:一种是单核细胞增生李斯特菌(LM)感染的小鼠模型,其中可追踪到对LM表达抗原(李斯特菌溶血素O,LLO)特异的CD8 + T细胞;另一种是小鼠皮肤移植模型,其中CD8 + T细胞介导跨越MHC I类(D(d))差异的排斥反应。在经LM免疫的小鼠中,LLO特异的CD8 + T记忆细胞在照射后消失,在照射后1 - 3天用减毒株快速重新接种可使其得以保留,并且这些小鼠在随后的野生型LM攻击中存活下来。一种基因“挽救特征”鉴定出一组在照射和挽救后维持或上调的免疫相关mRNA。其中许多因子,包括IL - 36γ、dectin - 2(Clec4n)和mir101c,在小鼠仅暴露于亚致死剂量γ射线后迅速上调,并由早期而非晚期的挽救得以维持。这些因子将被评估为潜在的治疗方法,以替代个体疫苗,用于在亚致死剂量γ射线照射后全面挽救CD8 + T记忆细胞反应。皮肤同种异体移植模型与LM模型相似,即暴露于亚致死剂量γ射线照射的小鼠中加速的D(d)皮肤同种异体移植排斥反应消失,但在照射后1 - 4天输注表达同种异体D(d)的骨髓细胞可保留CD8 + T记忆介导的加速排斥反应,这进一步表明先天免疫反应对于γ射线照射后挽救CD8 + 记忆T细胞可能并非总是必不可少的。