Sahlberg Anna S, Granfors Kaisa, Penttinen Markus A
Department of Bacterial and Inflammatory Diseases, National Public Health Institute, Turku, Finland.
Adv Exp Med Biol. 2009;649:235-44. doi: 10.1007/978-1-4419-0298-6_17.
HLA-B27 is a risk factor closely associated to spondyloarthropathies (SpA). One form of SpA is reactive arthritis (ReA), which develops as a complication after certain bacterial infections (e.g., Salmonellae, Yersiniae, Shigellae, Campylobacteriae and Chlamydiae). The development of infection-triggered complication is a complex train of events between the triggering bacteria and the host. Since most of the patients suffering from ReA are HLA-B27 positive, it has been proposed that HLA-B27 may modulate the interaction between ReA-triggering bacteria and host cell. Besides antigen presenting function, HLA-B27 displays other unusual properties that might be of importance in the development of ReA. These properties (homodimer formation and misfolding of HLA-B27 heavy chain in the endoplasmic reticulum (ER)) may trigger ER-stress signaling pathways in host cell, which in turn may modulate cell signaling in favor of ReA-triggering bacteria. Here we summarize the observations of HLA-B27 modulating the interaction between ReA-triggering bacteria and host cell and discuss potential mechanisms behind the interaction.
HLA - B27是与脊柱关节病(SpA)密切相关的一个风险因素。SpA的一种形式是反应性关节炎(ReA),它是在某些细菌感染(如沙门氏菌、耶尔森氏菌、志贺氏菌、弯曲杆菌和衣原体)后作为一种并发症而发生的。感染引发的并发症的发展是触发细菌与宿主之间一系列复杂的事件。由于大多数患有ReA的患者HLA - B27呈阳性,因此有人提出HLA - B27可能调节ReA触发细菌与宿主细胞之间的相互作用。除了抗原呈递功能外,HLA - B27还表现出其他可能在ReA发展中起重要作用的异常特性。这些特性(在内质网(ER)中形成HLA - B27重链的同型二聚体和错误折叠)可能触发宿主细胞中的内质网应激信号通路,进而可能调节细胞信号传导,有利于ReA触发细菌。在这里,我们总结了关于HLA - B27调节ReA触发细菌与宿主细胞之间相互作用的观察结果,并讨论了这种相互作用背后的潜在机制。