The immunological significance of the ST2L/IL-33 interaction in obesity-associated inflammation and diabetes

Abstract

Low-grade chronic inflammation is considered as a major determinant
governing obesity and its progression to insulin resistance and type II
diabetes. Recent animal studies suggest that Th1 cells and cytotoxic T
cells are involved in the attraction of proinflammatory adipose tissue
macrophages, which are a major cause of adipose tissue inflammation,
and that Th2 cells are protective from such inflammation. The ST2L
molecule is expressed on the surface of macrophages, monocytes and
Th2 cells. The ligand for ST2L is IL-33. It has been shown that murine
IL-33 acts as a chemoattractant for Th2 cells and induces Th2-associated
cytokine production. In addition, IL-33-treated DCs stimulate
naive CD4+ T cells to produce robust IL-5 and IL-13. Therefore, ST2L/
IL-33 interaction may play a critical role in the induction, maintenance
and recruitment of protective Th2 cells in the adipose tissue. However,
the role of the ST2L/IL-33 pathway in obesity-associated adipose tissue
inflammation and diabetes has not been determined. We aimed in this
study to compare the expression level of ST2L and IL-33 in lean and
obese individuals with and without diabetes.
Plasma, serum, peripheral blood mononuclear cells, and adipose
tissue biopsies were isolated from adult lean and obese subjects with
and without diabetes, and assessed using immunological assays such as
ELISA, Flow Cytometry and Immunohistochemistry. Data on the
expression level of ST2L and IL-33 will be presented. Understanding of
the significance of the ST2L/IL-33 interaction may help in the
prevention of obesity-associated adipose tissue inflammation and
hence diabetes.