Abstract: | Antibodies against type II collagen (anti-CII) are arthritogenic and have a crucial role in the initiation of collagen-induced
arthritis. Here, we have determined the dependence of T and B cells in collagen-antibody-induced arthritis (CAIA) during different
phases of arthritis. Mice deficient for B and/or T cells were susceptible to the CAIA, showing that the antibodies induce
arthritis even in the absence of an adaptive immune system. To determine whether CII-reactive T cells could have a role in
enhancing arthritis development at the effector level of arthritis pathogenesis, we established a T cell line reactive with
CII. This T cell line was oligoclonal and responded to different post-translational forms of the major CII epitope at position
260–270 bound to the Aq class II molecule. Importantly, it cross-reacted with the mouse peptide although it is bound with lower affinity to the Aq molecule than the corresponding rat peptide. The T cell line could not induce clinical arthritis per se in Aq-expressing mice even if these mice expressed the major heterologous CII epitope in cartilage, as in the transgenic MMC (mutated
mouse collagen) mouse. However, a combined treatment with anti-CII monoclonal antibodies and CII-reactive T cells enhanced
the progression of severe arthritis. |