Open AccessAnti-CD25 Antibody Treatment of Mice Vaccinated and Challenged withBorreliaspp. Does Not Exacerbate Arthritis but Inhibits Borreliacidal Antibody Production
Author(s) -
Dean T. Nardelli,
Thomas F. Warner,
Steven M. Callister,
Ronald F. Schell
Publication year - 2006
Publication title -
clinical and vaccine immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.649
H-Index - 77
eISSN - 1556-6811
pISSN - 1556-679X
DOI - 10.1128/cvi.00137-06
Subject(s) - immunology , borrelia burgdorferi , il 2 receptor , antibody , vaccination , immune system , arthritis , borrelia , virology , antibody titer , biology , microbiology and biotechnology , medicine , titer , t cell
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 inBorrelia -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 inBorrelia -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 toBorrelia infection following vaccination.