Trauma, hemorrhagic shock, and burns initiate cellular immune responses with detrimental effects on the clinical outcome of trauma patients.

In the early phase after trauma, overwhelming inflammation causes neutrophil activation and subsequent organ damage, caused by neutrophil, that can result in adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF).

In the later phase after trauma, suppressive mediators found in the circulation of patients decrease the ability of lymphocytes to protect the trauma victim from invading microorganisms. This can lead to severe infections and sepsis that are major reasons for trauma deaths.

Our group has focused on the cellular and molecular mechanisms that are involved in the cellular immune response to trauma as well as novel therapeutic approaches to modulate this response. Learn more about the different research projects:

  • Gamma-Delta T Cells and Resolution of Inflammation
  • Neutrophil Activation and Inflammation
  • Hyertonic Modulation of the Immune Response
  • Purinergic Control of Neutrophil Chemotaxis
  • T Cell Activation and Dysfunction
  • Purinergic Signaling

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