Hellwig S M, van Spriel A B, Schellekens J F, Mooi F R, van de Winkel J G
Laboratory for Infectious Diseases Research, National Institute of Public Health and the Environment, Bilthoven, University Medical Center, Utrecht, The Netherlands.
Infect Immun. 2001 Aug;69(8):4846-50. doi: 10.1128/IAI.69.8.4846-4850.2001.
Infection with Bordetella pertussis, the causative agent of pertussis (whooping cough) in humans, is followed by the production of antibodies of several isotypes, including immunoglobulin A (IgA). Little is known, however, about the role of IgA in immunity against pertussis. Therefore, we studied targeting of B. pertussis to the myeloid receptor for IgA, FcalphaRI (CD89), using either IgA purified from immune sera of pertussis patients or bispecific antibodies directed against B. pertussis and FcalphaRI (CD89 BsAb). Both IgA and CD89 BsAb facilitated FcalphaRI-mediated binding, phagocytosis, and bacterial killing by human polymorphonuclear leukocytes (PMNL) and PMNL originating from human FcalphaRI-transgenic mice. Importantly, FcalphaRI targeting resulted in enhanced bacterial clearance in lungs of transgenic mice. These data support the capacity of IgA to induce anti-B. pertussis effector functions via the myeloid IgA receptor, FcalphaRI. Increasing the amount of IgA antibodies induced by pertussis vaccines may result in higher vaccine efficacy.
人类百日咳（百日咳）的病原体百日咳博德特氏菌感染后，会产生包括免疫球蛋白A（IgA）在内的几种同种型抗体。然而，关于IgA在抗百日咳免疫中的作用知之甚少。因此，我们使用从百日咳患者免疫血清中纯化的IgA或针对百日咳博德特氏菌和FcalphaRI（CD89）的双特异性抗体，研究了百日咳博德特氏菌对IgA的髓样受体FcalphaRI（CD89）的靶向作用。IgA和CD89双特异性抗体均促进了FcalphaRI介导的人多形核白细胞（PMNL）以及源自人FcalphaRI转基因小鼠的PMNL的结合、吞噬作用和细菌杀伤。重要的是，FcalphaRI靶向导致转基因小鼠肺部细菌清除增强。这些数据支持了IgA通过髓样IgA受体FcalphaRI诱导抗百日咳博德特氏菌效应功能的能力。增加百日咳疫苗诱导的IgA抗体量可能会提高疫苗效力。
