Role of Leukocyte Immunoglobulin G Receptors in Vaccine-Induced Immunity to Streptococcus pneumoniae

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http://www.journals.uchicago.edu/JID/journal/issues/v187n11/30037/brief/30037.abstract.html

The Journal of Infectious Diseases    2003;187:1686-1693
© 2003 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2003/18711-0002$15.00

 

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MAJOR ARTICLE

Role of Leukocyte Immunoglobulin G Receptors in Vaccine-Induced Immunity to Streptococcus pneumoniae

Eirikur Saeland,1 Jeanette H. W. Leusen,1 Gestur Vidarsson,1 Wietse Kuis,2 Elisabeth A. M. Sanders,2 Ingileif Jonsdottir,4 and Jan G. J. van de Winkel1,3

Departments of 1Immunology and 2Pediatric Immunology, University Medical Center Utrecht, and 3Genmab, Utrecht, The Netherlands; 4Department of Immunology, Landspitali-University Hospital, Reykjavik, Iceland

 

Received 11 September 2002; accepted 31 December 2002; electronically published 12 May 2003.

Members of the leukocyte immunoglobulin (Ig) G receptor (FcγR) family play a key role in antibody-mediated phagocytosis and can either enhance antigen presentation or down-modulate immune responses. We studied immune responses to a pneumococcal conjugate (pneumococcal polysaccharide serotype 1 [PPS1]–tetanus toxoid) and antibody-mediated protection in mice deficient for individual FcγRs and complement receptor 3 (CR3). FcR γ chain–deficient (FcR γ chain-/-) mice, which lack expression of both FcγRI and III, had significantly lower anti-PPS1 IgG2b and IgG3 responses than did wild-type mice, whereas FcγRII-deficient (FcγRII-/-) mice had significantly higher IgG2a and IgG3 titers. Wild-type and FcγRII-/- mice were protected against infection with pneumococcal serotype 1, whereas immunized FcR γ chain-/- and FcγRIII-deficient mice were not. Immunized CR3-deficient mice were protected against disease, and complement depletion had little effect on protection. These data indicate that activatory leukocyte FcγR, but not FcγRII (a murine homologue of human FcγRIIb), contributes to IgG-mediated protection against pneumococcal disease.

 


     Animal experiments were performed according to institutional and national guidelines.
     Financial support: University Medical Center Utrecht (Wilhelmina Kinderzickenhuis–STER grant); Netherlands Organization for Scientific Research (grant 901-07-229 to J.H.W.L.).

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