Several biologic agents including anti-tumor necrosis factor alpha (anti-TNF-α) drugs, anti-integrins, and antibodies to the p40 subunit of IL12/23 are approved for induction and maintenance of remission of IBD.
In the last years the role of IL-9 in autoimmune diseases such as rheumatic diseases and inflammatory bowel disease gained importance since the increased expression of this cytokine has been observed in animal models of intestinal inflammation and in groups of patients with ulcerative colitis.
Interleukin-23 (IL-23), a heterodimeric cytokine of covalently bound p19 and p40 proteins, has recently been closely associated with development of several chronic autoimmune diseases such as psoriasis, psoriatic arthritis or inflammatory bowel disease.
Although IL-9 has been recognized as a classical Th2-related cytokine, recent studies have indicated that IL-9-producing cells contribute to a group of autoimmune disorders including systemic lupus erythematosus (SLE), multiple sclerosis (MS), inflammatory bowel diseases (IBD), rheumatoid arthritis (RA) and psoriasis.
Furthermore, it was also demonstrated that IL-9 promotes Th17 cell-mediated tissue pathology in EAE and it compromises the barrier functions of the gut in IBD.
The blockade of IL-9 was suited to significantly ameliorate the disease activity and severity in experimental models of inflammatory bowel disease thereby suggesting that targeting IL-9 might function as a novel targeted approach for therapy.
Systemic IL9 was significantly lower in healthy individuals [9 pg/mL (95%CI: 8.2-10)] than in patients with inflammatory bowel disease (IBD): both inactive [14.3 pg/mL (11.9-19.9)] and active [27.6 pg/mL (24.5-32), <i>P</i> < 0.0001].
Recent genomic studies have identified genetic variants in the IL12B gene, which encodes the p40 subunit shared by interleukin 12 and interleukin 23, as susceptibility loci for inflammatory bowel disease (IBD).