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Clinical and Diagnostic Laboratory Immunology, November 2004, p. 1075-1084, Vol. 11, No. 6
1071-412X/04/$08.00+0     DOI: 10.1128/CDLI.11.6.1075-1084.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Association of CD4+ CD25+ T Cells with Prevention of Severe Destructive Arthritis in Borrelia burgdorferi-Vaccinated and Challenged Gamma Interferon-Deficient Mice Treated with Anti-Interleukin-17 Antibody

Dean T. Nardelli,1,2 Matthew A. Burchill,1,2 Douglas M. England,3,4 Jose Torrealba,4,5 Steven M. Callister,6 and Ronald F. Schell1,2,7*

Wisconsin State Laboratory of Hygiene,1 Departments of Bacteriology,2 Medical Microbiology and Immunology,7 Pathology and Laboratory Medicine,4 Surgery, University of Wisconsin,5 Department of Pathology, Meriter Hospital, Madison,3 Microbiology Research Laboratory and Department of Infectious Diseases, Gundersen Lutheran Medical Center, La Crosse, Wisconsin6

Received 14 May 2004/ Returned for modification 13 July 2004/ Accepted 22 July 2004

CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-{gamma}°) C57BL/6 mice challenged with the Lyme spirochete. When B. burgdorferi-vaccinated and challenged IFN-{gamma}° mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. Furthermore, histopathologic examination showed the mice to be free of destructive arthritis. When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. More importantly, severe destructive arthropathy was induced. In addition, delayed administration of anti-CD25 antibody decreased the severity of the arthritis. These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi.

* Corresponding author. Mailing address: University of Wisconsin, Wisconsin State Laboratory of Hygiene, 465 Henry Mall, Madison, WI 53706. Phone: (608) 262-3634. Fax: (608) 265-3451. E-mail: RFSchell{at}facstaff.wisc.edu.

Clinical and Diagnostic Laboratory Immunology, November 2004, p. 1075-1084, Vol. 11, No. 6
1071-412X/04/$08.00+0     DOI: 10.1128/CDLI.11.6.1075-1084.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Nardelli, D. T., Callister, S. M., Schell, R. F. (2008). Lyme Arthritis: Current Concepts and a Change in Paradigm. CVI 15: 21-34 [Full Text]  
  • Vojdani, A., Erde, J. (2006). Regulatory T Cells, a Potent Immunoregulatory Target for CAM Researchers: Modulating Tumor Immunity, Autoimmunity and Alloreactive Immunity (III). Evid Based Complement Alternat Med 3: 309-316 [Abstract] [Full Text]  
  • Nardelli, D. T., Cloute, J. P., Luk, K. H. K., Torrealba, J., Warner, T. F., Callister, S. M., Schell, R. F. (2005). CD4+ CD25+ T Cells Prevent Arthritis Associated with Borrelia Vaccination and Infection. CVI 12: 786-792 [Abstract] [Full Text]  


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