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Short‐term depletion of regulatory T cells converts self‐limiting arthritis into a chronic disease
Author(s) -
Kamradt Thomas,
Bruns Lisa,
Frey Oliver,
Reichel Andreas,
Morawietz Lars
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1073.1
Subject(s) - arthritis , foxp3 , il 2 receptor , medicine , immunology , immunization , regulatory t cell , inflammation , t cell , inflammatory arthritis , antibody , immune system
Background: we have established a new arthritis model, induced by immunization of normal mice with the glycolytic enzyme glucose‐6‐phosphate isomerase (G6PI) (Schubert et al. J. Immunol 2004;172:4503). Arthritis occurs in > 90% of the animals from d9 after the immunization and is usually self‐limiting within 30–40 days. We examined if regulatory T cells (Treg) were involved in the resolution of arthritis. Results: Injection of anti‐CD25 antibody on d‐11 and –8 before immunization resulted in a massive yet transient reduction of CD25 + FoxP3 + Treg. The percentage of Treg was normal at d12 after immunization i.e. early during the course of arthritis. This transient depletion affected the disease course profoundly, resulting in chronic‐destructive arthritis with histologically active inflammation over the whole follow‐up period (80d). Exacerbated arthritis was accompanied by increased T‐cell proliferation and increased numbers of IL‐17 producing T cells. Conclusions: CD25 + FoxP3 + Treg may not be effective in the resolution of ongoing arthritis. Rather, they seem to act in the induction phase of the disease by controlling the extent of T cell activation and differentiation.