Immunobiology and Stress Response Laboratories
- Dr. Carol Miller-Graziano, Director
The overall laboratory hypothesis is that unbalanced monocyte differentiation to inflammatory macrophage versus immunostimulatory dendritic cells results in cytokine shock and immunosuppression in traumatic patients. Post injury alterations in monocyte (MØ) receptor expression and stimulation are examined at the molecular (PCR, RPA, Microarray) cell expression (flow cytometry) and signal transduction levels assessed as pivotal in altered MØ differentiation. Early post injury mediators like prostaglandins and heat shock proteins are being assessed as triggers for these receptor changes. The induction of anergic and/or regulatory T lymphocytes by dysfunctional dendritic
cells is explored. Altered T cell activation, apoptosis and function are also assessed in molecular and signal transduction experiments. Regulatory and anergic T cells are being distinguished by unique receptor expression and signaling. Finally, in combination with 11 other medical centers including Stanford, Harvard, Washington U., Northwestern, and the University of Washington, we are identifying chemokine and other surface phenotypic markers for patients' developing immunoaberrances. Microarray analysis is also being used to identify novel targets for immunomodulation in these patients with systemic and chronic inflammatory pathology.
Stress Response Faculty Investigators - Projects
- Dr. Paul Bankey, Chief Division Acute Care - Epidermalogical and genetic changes in major trauma patients; Neutrophil activation and derangement after trauma.
- Technical Support: LeAnne Staples, Mita De, Sanjukta Bandyopadhyey.
- Instructor: Gautam Bandyopadhyey.
Administrative and Accounting Support:
- Joyce Krieger, Mariellen Blossom, Lynn Atene
Research Grant Support:
- Is Aberrant Monocyte Stimulation Pivotal in Post-Trauma MODS?
NIH - NIGMS, Carol Miller-Graziano, PI, Krzysztof Laudanski, Co-PI.