B cell depletion remedy STAT inhibition is successful inside the remedy of various autoimmune disorders. Even so, this treatment is shown to be connected with greater chance of adverse effects such as opportunistic infections. Therefore, in this study, we made and analyzed the Arthritis Research & Therapy 2012, Volume 14 Suppl 1 selective depletion treatment of pathogenic B cells using peptide tetramers in collagen induced arthritis model. Methods: Since the antigenic targets of pathogenic antibodies are identified in collagen induced arthritis model, we developed toxin conjugated peptide tetramers, which contained pathogenic epitope of mouse type II Collagen. The male DBA/1J mice were immunized with bovine CII and injected with toxin conjugated peptide tetramers on day 10 and day 20 after CIIimmunization.

We analyzed the effect of toxin conjugated peptide tetramers on the production of autoantibodies and clinical course of arthritis. Results: The incidence of arthritis was significantly lower in the tetramer treated group than within the control group. The mean serum antibody levels for CII did not differ significantly, but there were significant AMPK activators differences in the anti peptide antibodies over time. Conclusions: Peptide tetramer is efficient in the selective depletion of antigen specific B cells and decreased the incidence of arthritis in CIA model. As a result, depletion of antigen specific B cells using this strategy might be a new therapeutic intervention of autoimmune diseases.

P34 Peripheral tolerance induced by apoptotic cells and PD 1 CD8 T cells Hirotaka Kazama1, Tomonori Iyoda1, Satoko Yokoyama1, Kayo Inaba1, Thomas A Ferguson2, Shin Yonehara1 Mitochondrion 1Department of Biostudies, Kyoto University Graduate School, Kyoto 606 8501 Japan, 2Department of Ophthalmology and Visual Science, Washington University School of Medicine, MO 63110 USA Arthritis Investigation & Treatment 2012, 14 34 Self tolerization in peripheral is critical to prevent autoimmune illnesses including arthritis and here we focus on the role of PD 1 in tolerance induction against the antigen associated with apoptotic cellsdelivered intravenously. We accessed delayed type hypersensitivity reaction against hapten as antigen specific immune response, in which the injection of TNP apoptotic cells i. v. suppressedDTH in wild type mice but we found not in PD 1 KO mice.

Adaptive transfer of CD8 T cells into PD 1 KO mouse from wild type mice tolerated with TNP apoptotic cells suppresses DTH. This result shows PD 1 functions on CD8 T cells for immune suppression. Additionally we neutralized the PD 1 with antibody to determine the phase when PD 1 functions for immune cyclic peptide synthesis tolerance by apoptotic cells, and identified PD 1functionsparticularly at the initial phase of antigen specific immune response. We are further studying the mechanism of suppressive role of PD 1 CD8 T cells that should be activated with apoptotic cells.