Establishing IL-33 as a Harnessable Regulatory and Reparative Damage-Associated Molecular Pattern (DAMP) in Transplantation

Presenter: Hēth Turnquist, PhD

Dr. Turnquist's research program elucidates immune-mediated mechanisms that can be harnessed for the benefit of individuals with tissue injury and organ dysfunction or failure. A primary focus area of his research program is the identification of how IL-33, acting as a damage-associated molecular pattern (DAMP) when released from damaged stromal cells, influences inflammation and tissue repair. These broadly applicable studies in his laboratory have been supported by funding from multiple NIH institutes (NHLBI, NIAID, NIAMS, NIGMS) as well as several foundations (AHA, AST, Roche). Through this support, Dr. Turnquist's research group has revealed that IL-33 is a potent immune modulator that stimulates both adaptive and innate immune cells expressing the IL-33 receptor, ST2, after transplantation to protect the allograft. In his talk, he will be describing his group's recent findings published in JCI that heart transplant-derived IL-33 is a novel regulatory DAMP that modulates the immunometabolism of graft-infiltrating recipient monocytes to limit their pro-inflammatory activity.  This mechanism was important to protect against chronic rejection. He will also show new data related to their recent findings revealing a related regulatory and reparative mechanism where IL-33 drives Treg secretion of cytokines that are instrumental in limiting local inflammatory responses and directing the myeloid compartment into reparative subsets after tissue injury.  

Recent articles from Dr. Turnquist:

• Graft IL-33 regulates infiltrating macrophages to protect against chronic rejection

• IL-33–mediated IL-13 secretion by ST2 + Tregs controls inflammation after lung injury

• Alarmins and Their Receptors as Modulators and Indicators of Alloimmune Responses