Department of Immunology, University of Pittsburgh, E1051, BSTWR, 200 Lothrop Street, Pittsburgh, PA 15261, USA.
Immunol Res. 2011 Aug;50(2-3):255-60. doi: 10.1007/s12026-011-8221-2.
For over 100 years, it has been established that tumor-specific immune responses can frequently be detected in the tumor-bearing host. Whether or not these immune responses are capable of controlling the growth of the tumor is influenced by many factors. However, the mechanism by which the immune responses are initiated in the first place has remained a dilemma. In this chapter, we present evidence that heat shock protein-peptide complexes released by tumor cells are the entity responsible for initiating the immune responses. Interaction of the extracellular HSP with its receptor CD91 is necessary for priming the immune response. We propose that the disruption of the HSP-CD91 interaction may be an active mechanism by which tumors prevent the generation of immune responses against it.
一百多年来，人们已经确定，在肿瘤患者体内经常可以检测到肿瘤特异性免疫反应。这些免疫反应是否能够控制肿瘤的生长受到许多因素的影响。然而，免疫反应最初是如何被引发的机制仍然是一个难题。在本章中，我们提供的证据表明，肿瘤细胞释放的热休克蛋白-肽复合物是引发免疫反应的实体。细胞外 HSP 与受体 CD91 的相互作用对于启动免疫反应是必要的。我们提出，破坏 HSP-CD91 相互作用可能是肿瘤防止针对其产生免疫反应的一种主动机制。
