Primary cultured T cell vaccine for adjuvant arthritis (AA), collagen-induced arthritis (CA) and arthritis in HTLV-1 pX-transgenic mice as models of rheumatoid-like arthritis: dominancy of the roles of T cells or humoral factors in the pathogenesis of CA and pX-transgenic arthritis

It has been reported that a T cell vaccine is capable of regulating auto-reactive T cells, and may be used for protection against and treatment of adjuvant arthritis (AA), but no reports have appeared regarding other forms of autoimmune arthritis. In this paper, we aimed for protection against and treatment of collagen-induced arthritis (CA) and arthritis induced in HTLV-1 pX-transgenic mice (pX-A) with a T cell vaccine as another model of autoimmune arthritis, in addition to a parallel study on AA. Drained lymph node lymphocytes were cultured in eitherMycobacterium tuberculosis, type II collagen or in an anti-CD3 antibody immobilized dishes for a total of 7 days. These cells were then fixed with 0.5% glutaraldehyde and used as a T cell vaccine. This was applied in the following five groups: protection and treatment of AA, protection (tolerance induction) and treatment of CA, and treatment of pX-a. The effects of a T cell vaccine were examined as: (i) an arthritis score, (ii) a histopathological examination of joint lesions, (iii) serum titers of anti-type II collagen antibodies and (iv) serum levels of several cytokines. In terms of the arthritis score, although the T cell vaccine was effective both in the protection of and treatment against AA, it was not effective for either CA or pX-A. The serum titers of anti-collagen antibodies were unchanged in the four groups examined. The serum levels of interleukin-1 β showed almost no differences in the four groups. Serum levels of tumor necrosis factor-α and interferon-γ were significantly higher in the pX-A treatment group. The T cell vaccine was effective in both protecting against and treating AA; however, it was not effective with regard to CA and pX-A. The possible dominancy of T cells in the pathogenesis of each autoimmune arthritis was discussed.