Department of Medicine, Division of Infectious Diseases, University of California, Irvine, USA.
J Infect Dis. 2011 Dec 1;204(11):1750-61. doi: 10.1093/infdis/jir638. Epub 2011 Oct 12.
Heterozygous states of hemoglobin (Hb) A and HbS (HbAS, sickle-cell trait) or HbC (HbAC) protect against Plasmodium falciparum malaria by unclear mechanisms. Several studies suggest that HbAS and HbAC accelerate the acquisition of immunity to malaria, possibly by enhancing P. falciparum-specific antibody responses.
We used a protein microarray representing 491 P. falciparum proteins expressed during exoerythrocytic and erythrocytic stages of the life cycle to test the hypothesis that HbAS and HbAC enhance the P. falciparum-specific IgG response compared with normal HbAA. Plasma samples were collected from Malian children aged 2-10 years before and after a 6-month malaria season and were probed against the microarray. Immunoglobulin G (IgG) profiles of children with HbAA (n = 106), HbAS (n = 15), and HbAC (n = 20) were compared.
Although the magnitude and breadth of P. falciparum-specific IgG responses increased with age and from before to after the malaria season in each antigen category, Hb type did not independently predict significant differences in P. falciparum-specific IgG profiles.
These data do not support the hypothesis that HbAS and HbAC protect against malaria by enhancing P. falciparum-specific antibody responses. It remains possible that HbAS and HbAC protect against malaria by enhancing antibody responses to antigens not studied here or through other immune mechanisms.
血红蛋白(Hb)A 和 HbS(HbAS,镰状细胞特征)或 HbC(HbAC)的杂合状态通过不明机制对恶性疟原虫疟疾具有保护作用。多项研究表明,HbAS 和 HbAC 可能通过增强疟原虫特异性抗体应答而加速对疟疾的免疫获得。
我们使用代表疟原虫生活史的红细胞外期和红细胞期表达的 491 种疟原虫蛋白的蛋白质微阵列,来检验 HbAS 和 HbAC 相较于正常 HbAA 是否增强疟原虫特异性 IgG 应答的假设。从马里儿童(年龄为 2-10 岁)中采集血浆样本,在疟疾季节前和后 6 个月分别进行收集,并对微阵列进行探测。对 HbAA(n = 106)、HbAS(n = 15)和 HbAC(n = 20)儿童的 IgG 图谱进行比较。
尽管在每个抗原类别中,疟原虫特异性 IgG 应答的幅度和广度随年龄和疟疾季节的变化而增加,但 Hb 类型并不能独立预测疟原虫特异性 IgG 图谱的显著差异。
这些数据不支持 HbAS 和 HbAC 通过增强疟原虫特异性抗体应答来保护疟疾的假设。HbAS 和 HbAC 可能通过增强对这里未研究的抗原或通过其他免疫机制的抗体应答来保护疟疾。