Artherosclerosis as an infectious, inflammatory and autoimmune disease.

well defined, thus facilitating the delineation of T-cell specificities (J. Sieper, Benjamin-Franklin Free University, Berlin, Germany) that might contribute to the conversion of immunity into joint pathology. B.T. Huber (Tufts University School of Medicine, Boston, MA, USA) demonstrated that the Borrelia burgdorferi outer surface protein A (OspA) plays a major role in the induction of crossreactive T-cell responses to the ‘self ’ determinant leukocyte integrin LFA-1 (Ref. 5). OspA-specific T-cell clones could be cultured from the synovial fluid of patients with treatment-resistant Lyme arthritis. Upon stimulation with an LFA-1 peptide, 7–10% of these T cells proliferated and produced Th2 cytokines, in particular IL-13. Interestingly, these dual specificity T-cell clones were predominantly restricted to the ‘shared epitope’ (HLADRB1*01 or HLA-DRB1*04) that is also associated with aggressive forms of RA. Thus, the data indicate that the potential pathogenic role of a molecular mimicry between OspA and LFA-1 is to drive antibody-mediated immunity.