Table 1

IL-6 signalling blockade in different disease models




Experimental arthritis

IL-6 is required for the development of collagen induced arthritis


IL-6-/- and IL-6+/+ mice

IL-6 plays a key role in the development of antigen induced arthritis


IL-6-/- mice

Blockade of IL-6 receptor ameliorates joint disease in murine collagen induced arthritis


Soluble IL-6 receptor governs IL-6 activity in antigen-induced arthritis: blockade of arthritis severity by soluble gp130


IL-6-/- mice


Blockade of IL-6 trans-signalling suppresses T cell resistance against apoptosis in chronic intestinal inflammation


Neutralization of sIL-6R by a gp130-Fc fusion protein

IL-6 is required for the development of Th1 cell mediated murine colitis


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


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


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


Toxoplasma gondii


Candida albicans


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.

Gabay Arthritis Research & Therapy 2006 8(Suppl 2):S3   doi:10.1186/ar1917