ViewpointBypassing the antigen to control rheumatoid arthritis
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Cyclosporine A inhibits IL-15-induced IL-17 production in CD4<sup>+</sup> T cells via down-regulation of PI3K/Akt and NF-κB
2007, Immunology LettersCitation Excerpt :We also reported recently that CSA increases production of IL-10 from fibroblast-like synoviocytes, and that this is responsible for inhibiting the production of Th1 and proinflammatory cytokines, including IFN-γ, IL-2, IL-12, and TNF-α [30]. These data lead us to believe that CSA might be an appropriate immunosuppressant in balancing the Th1/Th2 phenotype of memory T cell in RA [31,32]. CSA might be reassessed as a drug acting by a new mechanism because the different receptors produce dissimilar signals via two distinct signaling pathways: (1) antigen-presenting cells contact the TCR, the TCR induces NFAT translocation into the nucleus, and NFAT binds the promoter of the IL-17 gene, causing expression of IL-17 and (2) IL-15 contacts IL-15R, γc of IL-15R mediates stimulation of PI3K/NF-κB, NF-κB translocates into the nucleus, and NF-κB binds the promoter of IL-17 gene, causing expression of IL-17.
Therapeutic relevance of altered cytokine expression
2001, CytokineRapid onset of cutaneous squamous cell carcinoma in patients with rheumatoid arthritis after starting tumor necrosis factor α receptor IgG1-Fc fusion complex therapy
2001, Journal of the American Academy of DermatologyBiologic agents and immunotherapy in rheumatoid arthritis
1998, Rheumatic Disease Clinics of North AmericaDifferentiation of naive CD4<sup>+</sup> T cells towards T helper 2 cells is not impaired in rheumatoid arthritis patients
2003, Arthritis Research and Therapy