IL-33 promotes GATA-3 polarization of gut-derived T cells in experimental and ulcerative colitis

Abstract

The study demonstrates that intestinal IL-33 is capable of inducing GATA-3 in mucosal T cells, and suggests that IL-33 is a key mediator of pathological TH2 and non-TH2-type responses in intestinal inflammation. Blocking IL-33 signaling could be a feasible option in the treatment of UC.

HMGB1 regulates IL-33 expression in acute respiratory distress syndrome

“…We suggest that IL-33 has a proinflammatory role in many inflammatory diseases even though the mechanisms of IL-33 expression, processing and secretion are not yet determined. IL-33 is considered to mainly induce the expression of Th2-type cytokines in atopic dermatitis and ulcerative colitis [38,39]. In addition, IL-33 can exacerbate inflammation responses associated with rheumatoid arthritis (RA) via enhancing the synthesis of autoimmune-related pro-inflammatory cytokines and chemokines [40].…”

The role of IL-33/ST2L signals in the immune cells

“…1). Mesenteric lymph node T cells stimulated with IL-33 have increased GATA3 expression, and show an IL-33 dose dependent increase in secreted Th2-type cytokines IL-4 and IL-5, whereas this effect is abolished by blocking IL-33 signaling [39]. As ST+ Th2 cells have higher responsiveness for IL-2 by increased CD25 expression [33], it provides better accessibility of the il4 locus in Th2 cells and allow for enhanced production of IL-4, IL-5, and IL-13 mRNA.…”

The IL-33/ST2 axis: Role in health and disease

“…Two murine colitis models, one induced by DSS treatment or the IL-10 deficient mice, showed increased colonic IL-33 levels that correlate with colitis score and induction of GATA-3, a master regulator gene of Th2 differentiation, in T cells from intestinal tissue [71].…”