Dissecting the multifactorial causes of immunodominance in class I-restricted T cell responses to viruses
Dissecting the multifactorial causes of immunodominance in class I-restricted T cell responses to viruses
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DOI：
10.1016/s1074-7613(00)80161-2
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发表时间：
2000-01-01
期刊：
影响因子：
32.4
通讯作者：
Yewdell, JW
中科院分区：
文献类型：
--
作者：
Chen, WS;Antón, LC;Yewdell, JW
在流感病毒感染后，小鼠T-CD 8+细胞对五种不同决定簇的应答数量在初次应答中变化超过50倍，但在二次应答中变化较小。令人惊讶的是，每个决定因素激发了高度多样性和高度敏感的T-CD 8+反应。病毒感染细胞的抗原处理效率低下，导致其中一个次显性决定簇的免疫原性较差。使用牛痘病毒过度表达I类肽复合物揭示了两个次显性决定簇的不良免疫原性反映了与TCR多样性或敏感性无关的T细胞应答的局限性。尽管表达大大增强，但当被牛痘病毒过表达时，免疫显性决定簇实际上免疫原性较低。免疫优势也受到T-CD 8+抑制对其他决定因素的反应的能力的决定因素特异性变化的调节。
Following influenza virus infection, the numbers of mouse T-CD8+ cells responding to five different determinants vary more than 50-fold in primary responses but less so in secondary responses. Surprisingly, each determinant elicits a highly diverse and highly sensitive T-CD8+ response. Inefficient antigen processing by virus-infected cells accounts for the poor immunogenicity of just one of the subdominant determinants. Over-expressing class I-peptide complexes using vaccinia virus revealed that the poor immunogenicity of two subdominant determinants reflects limitations in T cell responses unrelated to TCR diversity or sensitivity. Despite greatly enhanced expression, the immunodominant determinant is actually less immunogenic when overexpressed by vaccinia virus. Immunodominance is also modulated by determinant-specific variations in the capacity of T-CD8+ to suppress responses to other determinants.