Table 1.
IL-6 signalling blockade in different disease models
| 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 |
| Colitis | ||
| 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] |
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.