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
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