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Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107
Vaccination is the most effective way to control infectious diseases. A variety of microbial pathogens use antigenic variation, an immune evasion strategy that poses a challenge for vaccine development. To understand protective immune responses against such pathogens, we have been studying Borrelia hermsii, a bacterium that causes recurrent bacteremia due to antigenic variation. An IgM response is necessary and sufficient to control B. hermsii infection. We have recently found a selective expansion of B1b cells concurrent with the resolution of B. hermsii bacteremia. B1b cells from convalescent but not naive mice confer long-lasting immunity, but the Ag(s) driving the protective IgM responses is unknown. Herein we demonstrate that convalescent B1b cell-derived IgM recognizes complement factor H-binding protein (FhbA), a B. hermsii outer-surface protein and putative virulence factor that does not undergo antigenic variation and is expressed by all clinical isolates. A progressive increase in the IgM response to FhbA correlated with the kinetics of B1b cell expansion, diminished the severity of bacteremic episodes, and led to the eventual resolution of the infection. These data indicate that FhbA is a specific target for protective B1b cell responses. Ags recognized by B1b cells may be considered as an important component in vaccination strategies.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by National Institutes of Health Grant RO1 AI065750 (to K.R.A.).
2 Address correspondence and reprint requests to Dr. Kishore R. Alugupalli, Department of Microbiology and Immunology, Thomas Jefferson University, 233 South 10th Street, BLSB 726, Philadelphia, PA 19107. E-mail address: kishore.alugupalli{at}mail.jci.tju.edu
3 Abbreviations used in this paper: Vmp, variable major protein; AID, activation-induced cytidine deaminase; Btk, Bruton’s tyrosine kinase; CRASP-1, complement regulator-acquiring surface protein 1; EV, empty vector; FhbA, complement factor H-binding protein A; FO, follicular; IPTG, isopropyl β-D-thiogalactoside; LC-MS/MS, liquid chromatography/mass spectrometry/mass spectrometry; MZ, marginal zone; rFhbA, recombinant FhbA; xid, X-linked immunodeficient.
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