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Infection and Immunity, August 2001, p. 4846-4850, Vol. 69, No. 8
Laboratory for Infectious Diseases
Research,1 and Diagnostic Laboratory for
Infectious Diseases and Perinatal
Screening,4 National Institute of Public
Health and the Environment, Bilthoven, and Immunotherapy
Laboratory, Department of Immunology,2
Medarex Europe,3
Genmab,6 and Eijkman-Winkler
Institute,5 University Medical Center,
Utrecht, The Netherlands
Received 16 January 2001/Returned for modification 12 March
2001/Accepted 4 May 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,
Fc
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.8.4846-4850.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Immunoglobulin A-Mediated Protection against
Bordetella pertussis Infection
RI (CD89), using either IgA purified from immune sera of pertussis
patients or bispecific antibodies directed against B.
pertussis and Fc
RI (CD89 BsAb). Both IgA and CD89 BsAb
facilitated Fc
RI-mediated binding, phagocytosis, and bacterial
killing by human polymorphonuclear leukocytes (PMNL) and PMNL
originating from human Fc
RI-transgenic mice. Importantly, Fc
RI
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, Fc
RI. Increasing the amount of IgA antibodies
induced by pertussis vaccines may result in higher vaccine efficacy.
*
Corresponding author. Mailing address: Immunotherapy
Laboratory, University Medical Center Utrecht, KC02.085.2, Lundlaan 6, 3584 EA Utrecht, The Netherlands. Phone: 31.30.2504306. Fax:
31.30.2504305. E-mail: J.vandewinkel{at}lab.azu.nl.
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