IL-33 improves the suppressive capacity of human regulatory T cells

Abstract

One of the main problems that immunologists have not solved yet involves the immunosuppression of ongoing exacerbated responses, as in transplant rejection and autoimmune diseases. To overcome these difficulties, different approaches have been used including the administration of immunosuppressive drugs, monoclonal antibodies, and more recently, the utilization of cellular therapy. In this last strategy, huTregs have been proposed as a safe tool to control transplant rejection or collateral immune reactions such as GvHD. Tregs are a subtype of CD4+ T cells characterized by the expression of markers such as CD25, CD127, Foxp3, among others, and their capacity to induce immune tolerance. For this reason, huTregs have become an attractive target for their manipulation and application in the clinic. In this work, we used an established protocol for the expansion of peripheral blood-derived huTregs, adding IL-33 as a putative enhancer of huTregs function, due to its previously identified capacity for driving transplant tolerance. Here, we characterized the phenotype, expansion rate and suppressive function of huTregs 33 . Although IL-33 did not modify the expression of Tregs canonical markers nor their proliferative activity, it did potentiate their suppressive function. This remarkable observation may be driven in part by the up-regulation of the immune regulatory-related genes, Foxp3, Amphiregulin and ST2. Thus, huTregs 33 should be considered for pre-clinical and clinical studies.

Bone Marrow-Derived C-Kit+ Cells Improved Inflammatory IL-33/ST-2/ILC2 Axis in the Lung Tissue of Type 2 Diabetic Rats

“…Gajardo et al also demonstrated the enhancement of Treg suppressive function by IL-33 [32]. It is notable that the therapeutic effect of IL-33 on Treg has been suggested as a possible treatment tool in the selective treatment of type 1 diabetes [43].…”

“…For induction of type 2 diabetes, animals in diabetic groups were fed with a high-fat diet for one month followed by a low-dose intraperitoneal injection of streptozotocin (35 mg/kg) in a 0.1 M citrate buffer (pH 4.5) [32]. The high-fat diet includes speci c percentages of ingredients mentioned in Table 1.…”