Ulcerative colitis (UC) is a kind of inflammatory bowel disease (IBD) that characterized by recurrent colonic mucosal inflammation and constitutive dysregulation of cytokine production [
1]. Although the etiology of UC remains unclear, it may be related to the genetic and environmental factors, along with dysfunction of the host immune responses against gut microbiota [
2] among which, immunological factors are particularly important. Evidence suggest that defects in the apoptotic pathway of T cells and intestinal epithelial cells (IECs) are important in the pathogenesis of the disease. IECs play a crucial role in immune hemostasis through the barrier function as well as innate immune defense and ability to modulate intestinal immune responses [
3,
4]. Intestinal epithelial cells produce thymic stromal lymphopoietin (TSLP) cytokine with immunomodulatory properties. IEC-derived TSLP is produced in response to signals received from commensal bacteria which promote dendritic cells (DC) and macrophages with tolerogenic properties. IEC-derived TSLP also contributes to the development and function of regulatory T cell (Treg) responses at mucosal sites [
5,
6]. Besides anti-inflammatory and tolerogenic activity, TSLP seems to play a pro-inflammatory role. TSLP activates myeloid DCs and increases the expression of MHCII, CD80, CD83, and CD86 molecules on the surface of these cells. Activated myeloid DCs then stimulate naive T CD4
+ cells and induce inflammatory T helper 2 (Th2) cells through the development of type 2 cytokines and activation of noncanonical NF-κB signaling. TSLP can also act directly on T cells via promoting proliferation and differentiation of naive CD4
+ T cells to Th2 cells through the induction of IL-4 gene transcription. TSLP also stimulates cytokine production from mast cells, NKT cells, and eosinophils [
7,
8]. Impairment of TSLP production by IECs due to inappropriate DC activation, increasing production of pro-inflammatory cytokines, and development of intestinal inflammation causes intestinal disorders, such as IBD [
9‐
12]. Many studies indicate that TSLP and other cytokines that their receptors share common gamma chain play a main role in regulation the activity of immune cells and are thus important for therapeutic approaches [
4,
13‐
15].
Interleukin-33 (IL-33), a novel identified member of the IL-1 family, has been reported to be produced by several different cell types, such as fibroblasts, adipocytes, endothelial cells, and intestinal epithelial cells [
2,
16]. IL-33 plays a major role in improving and controlling the bowel inflammation, particularly in UC [
17]. IL-33 has a single domain that binds to its receptor, IL-1 receptor like 1 (IL1RL1), also known as suppression of tumorigenicity 2 (ST2), and eliminates intestinal parasite infections through the induction of Th2 cytokines, such as IL-13 and IL-5 [
18‐
21]. ST2 receptor is expressed on human and mice basophils, eosinophils, mast cells, monocytes, DCs, NKT cells, and Th2 lymphocytes [
22‐
24]. This cytokine induces development of tolerogenic DCs and macrophages and finally leads to induction of iTregs [
25]. In some studies, decreased levels of IL-33 and elevated levels of soluble ST2 (sST2), a decoy receptor of IL-33, was observed in sera from patients with IBD compared with healthy individuals [
17]. In fact, IL-33 has been considered as a cytokine with dual functions. In the normal conditions, it can promote macrophage polarization towards M2 phenotype and enhance TGF-β expression which is important in the induction of Tregs. In intestinal inflammation, however, IL-33 play its protective role by Th2 induction. The aim of this study was to determine the relative gene expression of TSLP and IL-33 in UC patients and healthy individuals.