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Clinical and Vaccine Immunology, August 2006, p. 884-891, Vol. 13, No. 8
1071-412X/06/$08.00+0 doi:10.1128/CVI.00137-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Wisconsin State Laboratory of Hygiene and Departments of,1 Comparative Biomedical Sciences,2 Bacteriology,3 Medical Microbiology and Immunology, University of Wisconsin,4 Department of Pathology, Veterans Administration Hospital, Madison,5 Microbiology Research Laboratory and Section of Infectious Diseases, Gundersen Lutheran Medical Center, La Crosse, Wisconsin6
Received 12 April 2006/ Returned for modification 9 May 2006/ Accepted 25 May 2006
CD4+ CD25+ T cells are a population of regulatory T cells responsible for the modulation of the immune response in several autoimmune and infectious disease models. We previously showed that adoptive transfer of enriched CD4+ CD25+ T cells also plays a major role in the prevention of arthritis in Borrelia-vaccinated (Borrelia burgdorferi isolate 297) and -challenged (B. bissettii) mice. Here, we present evidence that administration of anti-CD25 antibody at the time of challenge or at later intervals fails to enhance the development of severe destructive osteoarthropathy in Borrelia-vaccinated C57BL mice. However, Borrelia-vaccinated and -challenged mice receiving anti-CD25 antibody developed decreased borreliacidal antibody titers compared to vaccinated and challenged controls. These findings suggest that additional mechanisms besides CD4+ CD25+ T cells are involved in the regulation of the immune response to Borrelia infection following vaccination.
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