IL-33 receptor ST2 deficiency attenuates renal ischaemia–reperfusion injury in euglycaemic, but not streptozotocin-induced hyperglycaemic mice

Abstract

Our data suggest that the IL-33/ST2 pathway exerts differential effects depending on the glucose environment, opening-up new avenues for future research on alarmins and diabetes in ischaemia-related diseases.

The role of activation of KАTP channels on hydrogen sulfide induced renoprotective effect on diabetic nephropathy

“…In addition, in the diabetic group, UAE, and A/C ratio were significantly higher than in the control rats. These results come in line with (Sehnine et al, ).…”

“…In addition, in the diabetic group, UAE, and A/C ratio were significantly higher than in the control rats. These results come in line with (Sehnine et al, 2018). To explain the mechanisms beyond renal injury induced by diabetes induction; total NO, oxidative stress markers, and inflammatory markers measured in the renal tissue.…”

Pathophysiologic role of Interleukin-33/ST2 in Sjögren's syndrome

“…IL-33 acting as an alarmin triggers and amplify the activation of NKT cells through innate as well as adaptative immune responses. Similar to NK cell, NKT cells constitutively express on their surface the ST2 chain that is specific to the IL-33 receptor thereby contributing as a co-stimulatory agent to Th1 (IFN-γ), Th2 (IL-4) and Th17 (IL-17A) NK and NKT cell cytokine production [90,91]. In our study, we could not depict Th17 responses following either IL-12 or IL-23 stimulation of NK and NKT cells.…”

Emerging Roles of Interleukin-33-responsive Kidney Group 2 Innate Lymphoid Cells in Acute Kidney Injury

“…Several groups have generated IL1RL1-deficient mice for the genetic deletion of the IL-33 receptor, which is encoded by the IL1RL1 gene. Sehnine et al used the IL1RL1 knockout mice to demonstrate that streptozotocin (STZ)-induced hyperglycemic mice exhibited an increased urinary albumin excretion [77]. At 24 h post-IRI, the ST2 knockout mice exhibited markedly reduced plasma creatinine, blood urea nitrogen (BUN), and tubular injury.…”

“…At 24 h post-IRI, the ST2 knockout mice exhibited markedly reduced plasma creatinine, blood urea nitrogen (BUN), and tubular injury. However, this protective effect was mitigated in the ST2-induced diabetes mellitus (DM) mice [77]. This suggested that the high glucose environment may impair the IL-33/ST2-mediated renal protective function.…”