This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Feng, S.
Right arrow Articles by Barthold, S. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Feng, S.
Right arrow Articles by Barthold, S. W.

 Previous Article  |  Next Article 

Infection and Immunity, December 2003, p. 7211-7214, Vol. 71, No. 12
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.12.7211-7214.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Immunogenicity of Borrelia burgdorferi Arthritis-Related Protein

Sunlian Feng, Emir Hodzic, Kimberly Freet, and Stephen W. Barthold*

Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California at Davis, Davis, California 95616

Received 30 May 2003/ Returned for modification 16 July 2003/ Accepted 2 September 2003

Immunization against arthritis-related protein (Arp) elicits antibody in mice that resolves arthritis but is not protective against challenge with Borrelia burgdorferi. In mice immunized against Arp, an unrelated 37-kDa protein (P37-42), outer surface protein A (OspA), or glutathione S-transferase (GT) and then challenged by syringe or tick, only OspA conferred protection. Passive transfer of Arp antiserum into infected SCID mice induced arthritis resolution, but antisera to P37-42, OspA, GT, or six overlapping Arp peptide fragments did not. Results suggest that the arthritis-resolving immunogenicity is specific to Arp, but the relevant epitopes may be conformational.


* Corresponding author. Mailing address: Center for Comparative Medicine, University of California at Davis, One Shields Ave., Davis, CA 95616. Phone: (530) 752-1245. Fax: (530) 752-7914. E-mail: swbarthold{at}ucdavis.edu.

Editor: F. C. Fang


Infection and Immunity, December 2003, p. 7211-7214, Vol. 71, No. 12
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.12.7211-7214.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Pal, U., Wang, P., Bao, F., Yang, X., Samanta, S., Schoen, R., Wormser, G. P., Schwartz, I., Fikrig, E. (2008). Borrelia burgdorferi basic membrane proteins A and B participate in the genesis of Lyme arthritis. JEM 205: 133-141 [Abstract] [Full Text]  
  • Xu, Q., Seemanapalli, S. V., McShan, K., Liang, F. T. (2006). Constitutive Expression of Outer Surface Protein C Diminishes the Ability of Borrelia burgdorferi To Evade Specific Humoral Immunity. Infect. Immun. 74: 5177-5184 [Abstract] [Full Text]  
  • Xu, Q., Seemanapalli, S. V., Lomax, L., McShan, K., Li, X., Fikrig, E., Liang, F. T. (2005). Association of Linear Plasmid 28-1 with an Arthritic Phenotype of Borrelia burgdorferi. Infect. Immun. 73: 7208-7215 [Abstract] [Full Text]  
  • Hodzic, E., Tunev, S., Feng, S., Freet, K. J., Barthold, S. W. (2005). Immunoglobulin-Regulated Expression of Borrelia burgdorferi Outer Surface Protein A In Vivo. Infect. Immun. 73: 3313-3321 [Abstract] [Full Text]  
  • Wang, X., Ma, Y., Weis, J. H., Zachary, J. F., Kirschning, C. J., Weis, J. J. (2005). Relative Contributions of Innate and Acquired Host Responses to Bacterial Control and Arthritis Development in Lyme Disease. Infect. Immun. 73: 657-660 [Abstract] [Full Text]  
  • Liang, F. T., Yan, J., Mbow, M. L., Sviat, S. L., Gilmore, R. D., Mamula, M., Fikrig, E. (2004). Borrelia burgdorferi Changes Its Surface Antigenic Expression in Response to Host Immune Responses. Infect. Immun. 72: 5759-5767 [Abstract] [Full Text]