Fc Receptor-Mediated Immunity Against Bordetella pertussis

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, FcgammaRIIa (CD32) and Fcg...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2001-12, Vol.167 (11), p.6545-6551
Main Authors: Rodriguez, Maria Eugenia, Hellwig, Sandra M. M, Hozbor, Daniela F, Leusen, Jeanette, van der Pol, W. -Ludo, van de Winkel, Jan G. J
Format: Article
Language:English
Subjects:
AFc receptors
Antibodies, Bacterial - blood
Antibodies, Bacterial - physiology
Blood Bactericidal Activity
Bordetella pertussis
Bordetella pertussis - immunology
Fc receptors
Humans
Immunity, Cellular - immunology
Immunoglobulin A - blood
Immunoglobulin A - physiology
Immunoglobulin G - blood
Immunoglobulin G - physiology
Neutrophils - immunology
Neutrophils - microbiology
Opsonin Proteins - blood
Opsonin Proteins - physiology
Phagocytosis - immunology
Receptors, Fc - blood
Receptors, Fc - physiology
Receptors, IgG - blood
Receptors, IgG - physiology
Respiratory Burst - immunology
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Summary: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, FcgammaRIIa (CD32) and FcgammaRIIIb (CD16), working synergistically. Furthermore, these FcgammaR 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 FcalphaR (CD89). Simultaneous engagement of FcalphaRI and FcgammaR 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.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.167.11.6545