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. Author manuscript; available in PMC: 2009 Nov 1.
Published in final edited form as: Hum Immunol. 2008 Sep 21;69(11):781–789. doi: 10.1016/j.humimm.2008.08.283

Figure 3. Proposed mechanisms of CD8+ suppressor T cells (Ts) in rheumatoid arthritis (RA).

Figure 3

CD8+CD28−CD56+ Ts transferred into SCID-chimera mice transplanted with synovial tissues from RA patients suppress the tissue inflammation measured by proinflammatory cytokines and chemokine expression, downmodulating the expression of costimulatory molecules CD80 and CD86 on antigen-presenting cells (APC) and synovial fibroblast-like cells (FLS). Interleukin (IL)-16-secreting CD8+ Ts suppress the tissue inflammation in the same SCID-chimera model. IL-16 is a natural ligand of the CD4 molecule and induces CD4+ T-cell anergy. IL-16 also may induce or recruit CD4+CD25+Foxp3+ Tregs in the tissue. In a mice collagen-induced arthritis model (CIA), CD8+CD11c+ Ts induced by the administration of anti-4-1 BB monoclonal antibodies (mAb) secrete IFNγ and induce indoleamine 2,3-dioxygenase (IDO) in CD11b+ monocytes and CD11c+ dendritic cells (DC). IDO catabolizes tryptophan (Trp) into its catabolite such as kynurenine (Kyn). Depletion of Trp and generated Kyn exert immunosuppressive effects on effector CD4+ T cells. Abbreviations: MHC = major histocompatibility complex; T-cell receptor = TCR.