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A single epitope of  Leishmania  analog of the receptors for activated C kinase (LACK) from  Leishmania major , the polypeptide LACK 156–173 , is recognized by Vβ4 + /Vα8 +  T cells, and activate these cells that drives the subsequent T helper (Th)2 response. This study was undertaken to investigate the therapeutic potential of the LACK 156–173  epitope in murine autoimmune arthritis models. To explore the influence of the LACK 156–173  epitope on murine collagen antibody-induced arthritis, as well as its immunological mechanism, we vaccinated or treated mice with a LACK 156–173  epitope expression plasmid or polypeptide. The effect of LACK 156–173  epitope was then evaluated by clinical scores, histopathology, and quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Using flow cytometry, we measured the subsets and maturity of CD11c +  dendritic cells (DCs), as well as T cell polarization, in co-culture experiments. We also measured cytokine gene expression and production. The murine macrophage-like cell line RAW264.7 was used to identify the receptor for the epitope. Vaccination or treatment of the mice with the LACK 156–173  epitope expression plasmid or polypeptide ameliorated the severity of arthritis. qRT-PCR analysis revealed that the LACK 156–173  epitope improved the balance of effector T cells in synovial tissue compared to that in untreated arthritis controls. Toll-like receptor (TLR) 4 expression was diminished by LACK 156–173 . The epitope also influenced T cell polarization by regulating the differentiation, maturation, and functions of CD11c +  DCs and upregulating Jagged1 ligand expression. Blocking the mannose receptor (MR) significantly attenuated LACK 156–173  epitope-induced macrophage activation. Our data indicate that vaccination or treatment with a single microorganism epitope, LACK 156–173 , is a highly efficient therapy for murine autoimmune arthritis. The therapeutic effects are mediated by the regulation of the differentiation, maturation, and functions of DCs  via  MR, resulting in the upregulation of Jagged1 expression and Th2 cell polarization. Our results demonstrate the therapeutic potential of the LACK 156–173  epitope in rheumatoid arthritis.

A Single Microorganism Epitope Attenuates the Development of Murine Autoimmune Arthritis: Regulation of Dendritic Cells via the Mannose Receptor