An immunogenetic and molecular basis for differences in outcomes of invasive group A streptococcal infections
An immunogenetic and molecular basis for differences in outcomes of invasive group A streptococcal infections
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DOI：
10.1038/nm800
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发表时间：
2002-12-01
期刊：
影响因子：
82.9
通讯作者：
Low, DE
中科院分区：
文献类型：
--
作者：
Kotb, M;Norrby-Teglund, A;Low, DE
宿主遗传因素在赋予传染病易感性或保护性方面的作用已变得明显。感染A群链球菌可引起多种疾病，从咽炎到链球菌中毒性休克综合征。链球菌超抗原引发的炎症细胞因子的释放在侵袭性链球菌疾病中起关键作用。然而，感染同一菌株的个体可能表现出截然不同的症状。我们在这里报告了宿主的免疫遗传学影响侵袭性链球菌感染的结果，并证明了这些遗传关联的潜在机制。特异性人类白细胞抗原II类单倍型对严重全身性疾病具有强大的保护作用，而其他单倍型则增加了严重疾病的风险。DRB1*1501/DQB1*0602单倍型的患者反应显著降低，发生严重全身性疾病的可能性较小(P
The role of host genetic factors in conferring predisposition or protection in infectious diseases has become evident. Infection with group A streptococci causes a wide spectrum of disease ranging from pharyngitis to streptococcal toxic shock syndrome. The release of inflammatory cytokines triggered by streptococcal superantigens has a pivotal role in invasive streptococcal disease. However, individuals infected with the same strain can develop very different manifestations. We report here that the immunogenetics of the host influence the outcome of invasive streptococcal infection, and demonstrate the underlying mechanism for these genetic associations. Specific human leukocyte antigen class II haplotypes conferred strong protection from severe systemic disease, whereas others increased the risk of severe disease. Patients with the DRB1*1501/DQB1*0602 haplotype mounted significantly reduced responses and were less likely to develop severe systemic disease (P