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Table 1 IL-6 signalling blockade in different disease models

From: Interleukin-6 and chronic inflammation

Finding Ref. Comment
Experimental arthritis   
   IL-6 is required for the development of collagen induced arthritis [31] IL-6-/- and IL-6+/+ mice
   IL-6 plays a key role in the development of antigen induced arthritis [32] IL-6-/- mice
   Blockade of IL-6 receptor ameliorates joint disease in murine collagen induced arthritis [33]  
   Soluble IL-6 receptor governs IL-6 activity in antigen-induced arthritis: blockade of arthritis severity by soluble gp130 [34] IL-6-/- mice
   Blockade of IL-6 trans-signalling suppresses T cell resistance against apoptosis in chronic intestinal inflammation [30] Neutralization of sIL-6R by a gp130-Fc fusion protein
   IL-6 is required for the development of Th1 cell mediated murine colitis [35] C.B-17-scid mice transferred with CD45RBhigh CD4+ T anti-IL-6R mAb (MR16-1), used in a murine model of colitis
Modulating signaling   
   CIS3/SOCS3/SSI3 plays a negative role in STAT3 activation and intestinal inflammation [36] Development of colitis as well as STAT3 activation was significantly reduced in IL-6 deficient mice
   Induction of SOCS3/CIS3 as a therapeutic strategy for treating inflammatory arthritis [37] Recombinant adenovirus carrying the CIS3 cDNA injected periarticularly into the ankle joints of mice with antigen induced arthritis or collagen induced arthritis
Models of infection   
   IL-6 deficient mice are susceptible to:   
Listeria monocytogenes [38]  
Toxoplasma gondii [39]  
Candida albicans [40]  
  1. CIS, cytokine-induced SH2 protein; IL, interleukin; mAb, monoclonal antibody; sIL-6R, soluble IL-6 receptor; SOCS, suppressors of cytokine signaling; SSI, STAT-induced STAT inhibitors; STAT, signal transducer and activator of transcription; Th, T-helper.