Association of HLA-alleles with the immune regulation of chronic viral infections.
Association of HLA-alleles with the immune regulation of chronic viral infections.
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DOI：
10.1016/j.biocel.2012.05.003
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发表时间：
2012-08
期刊：
影响因子：
--
通讯作者：
Horton H
中科院分区：
文献类型：
--
作者：
Elahi S;Horton H
细胞毒性CD8 T淋巴细胞（CTL）具有消除病原体感染细胞的惊人能力。然而，如果不加控制，这些CTL可能对宿主组织造成破坏性的病理学。因此，CD8+效应T细胞与抗原呈递细胞和其他免疫细胞（如调节性T细胞（Tcells））相互作用，以调节效应细胞的进一步原位扩增和分化。这确保了对宿主的保护，同时使旁观者病理后果最小化。然而，在长期慢性感染期间，CTL通常失去效应子功能。在慢性病毒感染如HIV、HCV和HBV期间，多种抑制途径的诱导正在成为将效应CTL转化为耗尽的CTL的主要调节剂。在慢性病毒感染诱导衰竭的机制是这篇文章的重点。阻断抑制途径可能会恢复耗尽的CTL的功能能力，并代表慢性病毒感染中潜在的基于免疫的干预。
Cytotoxic CD8 T lymphocytes (CTLs) have an astonishing ability to eliminate pathogen-infected cells. However, if uncontrolled, these CTLs could cause devastating pathology to host tissues. CD8+ effector T cells, therefore, interact with antigen-presenting cells and other immune cells, such as regulatory T cells (Tregs), to regulate further on-site expansion and differentiation of the effector cells. This ensures protection of the host with minimal bystander pathological consequences. During prolonged chronic infections CTLs, however, often lose effector function. Induction of multiple inhibitory pathways is emerging as a major regulator converting effector CTLs into exhausted CTLs during chronic viral infections such as HIV, HCV and HBV. The mechanisms involved in induction of exhaustion during chronic viral infections are the focus of this article. Blockade of inhibitory pathways could potentially restore functional capabilities to exhausted CTLs and represents a potential immune-based intervention in chronic viral infections.
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