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Absence of In vitro Responses to Type II Collagen by Splenocytes from Arthritic BALB/ c Mice is Possibly Caused by Intrinsic CD25 + Regulatory Cells
Author(s) -
Bäckström F.,
Dahlgren U.
Publication year - 2008
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2008.02079.x
Subject(s) - medicine , splenocyte , autoantibody , arthritis , il 2 receptor , in vitro , immunology , type ii collagen , endocrinology , antibody , immune system , t cell , biology , biochemistry
Collagen‐induced arthritis‐resistant BALB/ c mice develop arthritis if a foreign protein is added to an emulsion of type II collagen (CII) and adjuvant. The IgG autoantibody activity to CII is increased, whereas no CII autoreactive T cells in vitro can be recorded. In this study, we have explored whether CD25 + cells inhibit T‐cell autoreactivity to CII. We also followed the IgG anti‐CII autoantibody activity and the IL‐6 level in serum during the development of arthritis. BALB/ c mice were coimmunized with bovine CII (BCII) and keyhole limpet haemocyanin (KLH) in complete Freund’s adjuvant and boostered 3 weeks later. Control animals were immunized with either BCII or KLH. Sera were collected prior to and during the development of arthritis and examined for IgG anti‐CII antibody activity and IL‐6 content. When all BCII–KLH immunized mice had developed arthritis, splenocytes were prepared, with and without CD25 + cells, and tested for BCII reactivity in vitro . The serum IgG, IgG1 and IgG2a anti‐CII antibody activities and the IL‐6 level were significantly higher in BCII–KLH immunized mice than in BCII‐immunized animals that failed to develop arthritis. The BCII‐specific IL‐2 secretion in vitro was significantly increased in CD25‐depleted splenocyte cultures prepared from arthritic BCII–KLH‐immunized mice. Development of arthritis in BALB/ c mice induced by coimmunization with BCII/KLH results in increased levels of circulating IL‐6 and IgG autoantibodies to CII. The arthritogenic BCII–KLH immunization potentiates BCII‐specific IL‐2 secretion by CD25‐depleted splenocytes, but CD25 + cells hamper the outcome of their action, at least in vitro .