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 CD45^RBhigh 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.

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