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The Journal of Immunology, 2001, 167: 6545-6551.
Copyright © 2001 by The American Association of Immunologists

Fc Receptor-Mediated Immunity Against Bordetella pertussis1

Maria Eugenia Rodriguez2,*,{ddagger}, Sandra M. M. Hellwig*,§, Daniela F. Hozbor{ddagger}, Jeanette Leusen*, W. -Ludo van der Pol3,* and Jan G. J. van de Winkel*,{dagger}

* Department of Immunology, and {dagger} Genmab, University Medical Center Utrecht, Utrecht, The Netherlands; {ddagger} Centro de Investigación y Desarrollo de Fermentaciones Industriales, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; and § Laboratory for Infectious Diseases Research, National Institute of Public Health and the Environment, Bilthoven, The Netherlands.

The relevance of specific Abs for the induction of cellular effector functions against Bordetella pertussis was studied. IgG-opsonized B. pertussis was efficiently phagocytosed by human polymorphonuclear leukocytes (PMN). This process was mediated by the PMN IgG receptors, Fc{gamma}RIIa (CD32) and Fc{gamma}RIIIb (CD16), working synergistically. Furthermore, these Fc{gamma}R triggered efficient PMN respiratory burst activity and mediated transfer of B. pertussis to lysosomal compartments, ultimately resulting in reduced bacterial viability. Bacteria opsonized with IgA triggered similar PMN activation via Fc{alpha}R (CD89). Simultaneous engagement of Fc{alpha}RI and Fc{gamma}R by B. pertussis resulted in increased phagocytosis rates, compared with responses induced by either isotype alone. These data provide new insights into host immune mechanisms against B. pertussis and document a crucial role for Ig-FcR interactions in immunity to this human pathogen.




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