Roper Rachel L
Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Methods Mol Biol. 2012;890:259-71. doi: 10.1007/978-1-61779-876-4_15.
Antigen presentation to T lymphocytes is the seminal triggering event of the specific immune response, and poxviruses encode immunomodulatory genes that disrupt this process. Discovery of viral proteins that interfere with steps in the antigen presentation process requires a robust, easily manipulated antigen-presenting and T lymphocyte response system. Use of fresh primary antigen-presenting cells (APC) is preferable because cell lines that can present antigen in vitro are often not representative of APC in vivo and are typically weak stimulators. To study immunomodulatory poxvirus genes, we have used infected primary rat macrophages to present a model antigen, the myelin basic protein peptide, to a cognate CD4+ RsL11 T cell clone. Using this system, viruses can be assessed for difference in immunomodulation, and viral gene functions may also be assayed by comparing effects of wild type virus and mutant viruses (e.g., a deletion in the putative immunomodulatory gene). While antigen presentation can be thought of as a single event, it can also be considered as a larger process comprising multiple steps including: antigen acquisition, antigen processing, peptide loading onto MHC molecules, transport to the surface, MHC binding to T cell receptor, interaction of costimulatory molecules, cell signaling, cytokine synthesis by both cells, and proliferation of antigen specific T lymphocytes. This system allows for the initial determination of whether there is a phenotype and then also allows the stepwise deconstruction of the system to analyze this process at several points to focus in on the mechanism of immunomodulation. We have used this model system to elucidate the function of a highly conserved but previously uncharacterized poxvirus gene that we showed was important for virulence in rodents. The experimental system developed should be broadly applicable to analyzing viral effects on immunity.
向T淋巴细胞呈递抗原是特异性免疫反应的起始触发事件,而痘病毒编码可破坏这一过程的免疫调节基因。发现干扰抗原呈递过程中各个步骤的病毒蛋白需要一个强大且易于操作的抗原呈递和T淋巴细胞反应系统。使用新鲜的原代抗原呈递细胞(APC)更为可取,因为能够在体外呈递抗原的细胞系通常不能代表体内的APC,而且通常是较弱的刺激物。为了研究免疫调节性痘病毒基因,我们使用感染的原代大鼠巨噬细胞向同源CD4 + RsL11 T细胞克隆呈递一种模型抗原,即髓鞘碱性蛋白肽。利用这个系统,可以评估病毒在免疫调节方面的差异,还可以通过比较野生型病毒和突变病毒(例如,假定的免疫调节基因缺失)的作用来检测病毒基因的功能。虽然抗原呈递可以被看作是一个单一事件,但也可以被视为一个包含多个步骤的更大过程,这些步骤包括:抗原获取、抗原加工、肽加载到MHC分子上、转运到表面、MHC与T细胞受体结合、共刺激分子的相互作用、细胞信号传导、两种细胞的细胞因子合成以及抗原特异性T淋巴细胞的增殖。这个系统允许初步确定是否存在表型,然后还允许逐步解构该系统,以便在几个点上分析这个过程,从而聚焦于免疫调节机制。我们已经使用这个模型系统阐明了一个高度保守但以前未被表征的痘病毒基因的功能,我们发现该基因对啮齿动物的毒力很重要。所开发的实验系统应该广泛适用于分析病毒对免疫的影响。