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Printable Handouts
Navigable Slide Index
- Introduction
- Humanized anti-IL-6R mAb therapy for JIA (1)
- Regulation of antibody response in vitro
- Interleukin-6
- IL-6 transgenic mouse
- Acute phase responses in IL-6 deficient mice
- IL-6 and IL-6 receptor interaction
- Cytokine receptor systems
- IL-6 signal transduction mechanism
- NF-IL6 induction of proteins, cytokines & viruses
- NF-IL6 induces HIV-1 replication
- Feedback regulation in IL-6 signaling
- Aberrant production of IL-6 in myxoma cells
- Synovial fluid IL-6 in Rheumatoid Arthritis patients
- Anti-IL6R Ab blocks IL-6 binding with the receptor
- Recombinant anti-human IL-6R mAb
- Anti-human IL-6R antibody (tocilizumab)
- Castleman's disease (CD)
- Features of Castleman's disease
- Lymph nodes in Castleman's disease
- KSHV/HHV8 in Castleman's disease
- Humanized anti IL-6 receptor Ab therapy
- Therapy of CD by humanized anti-IL-6R Ab
- Anti-IL-6R Ab improved laboratory abnormalities
- Rheumatoid Arthritis (RA)
- RA and IL-6 deficient mice
- ACR response rate using tocilizumab
- Tocilizumab therapy: Pre and post radiographs
- Inhibition of RANK ligand expression
- Inhibition of TRAP-positive osteoclast formation
- Disappearance of amyloid deposits in the colon
- The RADIATE study
- Juvenile Idiopathic Arthritis (JIA)
- Humanized anti-IL-6R mAb therapy for JIA (2)
- Systemic-onset Juvenile Idiopathic Arthritis
- Decrease in inflammation markers
- Decrease in fever episodes
- Physicians' assessment of disease activity
- Efficacy responses with tocilizumab therapy in JIA
- Tocilizumab in refractory relapsing polychondritis
- Treatment of reactive arthritis with tocilizumab
- Tocilizumab in polymyalgia rheumatica
- Tocilizumab treatment in systemic sclerosis
- MR16-1 in mouse model of scleroderma
- ACR response and serum IL-6 using tocilizumab
- IL-6 , TH17 and Treg cells
- Suppression of CII-induced arthritis (CIA)
- Suppression of IL-17 in MR16-1 treated mice
- No suppressive on Th17 induction with TNFR-Fc
- MR16-1 treatment reduces the incidence of EAE
- MR16-1 suppresses Th17 & Th1 development
- Experimental autoimmune uveoretinitis (EAU)
- Th17 development in IL-6 KO mice with EAU
- IL-17 and IFN-gamma KO mice develop EAU
- Regulatory T cells are important for inhibiting EAU
- TNF-alpha, IL-1 and IL-23 do not induce Th17 cells
- TNF-a, IL-1 & IL-23 don't inhibit Foxp3+ Treg cells
- Ahr is specifically induced by IL-6 and TGF-beta
- Ahr: aryl hydrocarbon receptor
- Induction of IL-17 in Ahr-deficient naive T cells
- Ahr specifically binds with Stat1 and Stat5
- Distinct roles of Stat family in Th17 differentiation
- Ahr gene deletion blocks the CIA development
- T cell-specific deletion of Ahr ameliorates the CIA
- Pro-inflammatory cytokines in Ahr KO mice
- Cytokine production in Ahr KO mice
- Research group
- Collaborations
Topics Covered
- IL-6 is a pleiotropic proinflammatory cytokine
- Its overproduction is involved in inflammatory autoimmune diseases including rheumatoid arthritis
- Blocking of IL-6 signals by anti-IL6 receptor antibody (Tocilizumab) shows therapeutic effect on various autoimmune diseases
- Tocilizumab exerts its effect by inhibiting the induction of a helper T cell subset (TH17)
- Aryl-hydrocarbon receptor (Ahr) is one of the essential molecule for the IL-6 mediated induction of TH17 cells
Talk Citation
Kishimoto, T. (2011, December 5). Interleukin-6: back to the future [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 21, 2024, from https://doi.org/10.69645/FHFX9461.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Tadamitsu Kishimoto has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.