Journal
ARTHRITIS RESEARCH & THERAPY
Volume 6, Issue 6, Pages R544-R550Publisher
BMC
DOI: 10.1186/ar1217
Keywords
arthritis; B cells; collagen type II; monoclonal antibodies; T cells
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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 A(q) class II molecule. Importantly, it cross-reacted with the mouse peptide although it is bound with lower affinity to the A(q) molecule than the corresponding rat peptide. The T cell line could not induce clinical arthritis per se in A(q)-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.
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