Table 2.
Interleukin | Th Subset | Function in IBD | Therapeutics |
---|---|---|---|
IL-1 | Th | Mediator of inflammation and tissue damage | Canakinumab (anti IL-1β) |
IL-17 | Th17 | T-cell activation to neutrophil mobilization and activation | Secukinumab, Ixekizumab, Brodalizumab |
IL-18 | Th17, Tregs | Intraepithelial cells proliferation, tissue regeneration, production of proinflammatory cytokines | - |
IL-33 | Tregs | Type 2 immune response, intraepithelial cells differentiation, intestinal inflammation | Tozarakimab |
IL-4 | Th2 | Induces IgE class-switch recombination in B cells; induces Th2 differentiation and IL-13 expression |
Pasolizumab (anti IL-4), Altrakincept (soluble Il-4R) |
IL-6 | Th17 | IEC proliferation and repair, crypt homeostasis | Olamkicept |
IL-10 | Tregs | Inhibits proinflammatory cytokine expression by innate/adaptive immune cells; STAT3-dependent signaling |
Recombinant IL-10 |
IL-11 | Macrophages | Activation of JAK/STAT signaling, tumor cell survival | - |
IL-13 | Th 2 | Impairs epithelial barrier function; promotes mucosal fibrosis via induction of TGFβ1 expression |
Anrukizumab, Lebrikizumab, Tralokizumab |
IL-22 | Th17, Th 22 | Enforces epithelial barrier function; stimulates expression of antimicrobial peptides, defensins |
Fezankizumab |
IL-9 | Th9 | Impairs mucosal wound healing; regulates epithelial cell proliferation, barrier function |
Enokizumab |
Adapted from [129].