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Department of Veterinary and Biomedical Science, The Pennsylvania State University, 115 Henning Building, University Park, Pennsylvania 16802,1 Center for Biologics Evaluation and Research, U.S. Food and Drug Administration, 8800 Rockville Pike, Bethesda, Maryland 208922
Received 9 May 2007/ Returned for modification 14 September 2007/ Accepted 15 February 2008
The threat of bioterrorist use of Bacillus anthracis has focused urgent attention on the efficacy and mechanisms of protective immunity induced by available vaccines. However, the mechanisms of infection-induced immunity have been less well studied and defined. We used a combination of complement depletion along with immunodeficient mice and adoptive transfer approaches to determine the mechanisms of infection-induced protective immunity to B. anthracis. B- or T-cell-deficient mice lacked the complete anamnestic protection observed in immunocompetent mice. In addition, T-cell-deficient mice generated poor antibody titers but were protected by the adoptive transfer of serum from B. anthracis-challenged mice. Adoptively transferred sera were protective in mice lacking complement, Fc receptors, or both, suggesting that they operate independent of these effectors. Together, these results indicate that antibody-mediated neutralization provides significant protection in B. anthracis infection-induced immunity.
Published ahead of print on 3 March 2008.
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
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| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
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