title: 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.
abstract: 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 degrees ) C57BL/6 mice challenged with the Lyme spirochete. When B. burgdorferi-vaccinated and challenged IFN-gamma degrees 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.
authors.affiliation: Wisconsin State Laboratory of Hygiene, University of Wisconsin, 465 Henry Mall, Madison, WI 53706, USA.
authors.forename: Dean T
authors.initials: DT
authors.lastname: Nardelli
authors.forename: Matthew A
authors.initials: MA
authors.lastname: Burchill
authors.forename: Douglas M
authors.initials: DM
authors.lastname: England
authors.forename: Jose
authors.initials: J
authors.lastname: Torrealba
authors.forename: Steven M
authors.initials: SM
authors.lastname: Callister
authors.forename: Ronald F
authors.initials: RF
authors.lastname: Schell
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage* / Q000276:immunology; D001170:Arthritis, Infectious / Q000276:immunology* / Q000473:pathology; D025065:Borrelia burgdorferi / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D007371:Interferon-gamma / Q000172:deficiency*; D020381:Interleukin-17 / Q000276:immunology; D008193:Lyme Disease / Q000150:complications / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control; D022123:Lyme Disease Vaccines / Q000008:administration & dosage / Q000276:immunology*; D051379:Mice; D018345:Mice, Knockout; D015375:Receptors, Interleukin-2 / Q000276:immunology*; D014611:Vaccination
chemical_list: D000911:Antibodies, Monoclonal; D020381:Interleukin-17; D022123:Lyme Disease Vaccines; D015375:Receptors, Interleukin-2; D007371:Interferon-gamma