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Nick Lukacs

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Primary Appointment: Pathology Department
Primary PIBS Dept.: Molecular and Cellular Pathology
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  Over the past several years the laboratory research has focused on the interrelationship of cytokines, chemokines, and leukocyte activation during asthmatic airway and Th1/Th2 cytokine immune responses. The development of clinically relevant mouse cockroach allergen and viral infection models that demonstrate a number of correlates to human disease have been successfully utilized to elucidate novel mechanisms of pulmonary disease. The areas investigated using these airway models include mast cell biology, eosinophilic inflammation, DC biology, and T lymphocyte differentiation. The laboratory has examined the role of pulmonary viral infections on exacerbation and increased development of allergic asthmatic responses. Identification of specific cytokine and chemokine mediators that are involved in each of these models have been elucidated and studies have correlated these pathways to clinical disease using physiological measurements in the lung. Recent studies in the laboratory have been focused on the function and signal transduction pathways of toll-like receptor molecules in pulmonary inflammation with a specific focus on DC and airway epithelial cells. The differential role of DC subsets, plasmacytoid and myeloid DC, for shaping the pulmonary immune response has been an additional focus of our laboratory investigations and have outlined the critical role innate immune molecules have during the development and maintenance of pulmonary disease.

Ongoing Laboratory Projects-

1. Role of chemokines and their receptors in pulmonary immune responses (allergic and viral).

2. Viral activation of TLRs determine the pulmonary immune environment by immune (DC subsets) and non-immune cells.

3. Differential expression of TLR-induced notch ligands and their receptors in determining immune responses during acute and chronic pulmonary immune responses.

3. The role of stem cell factor (SCF) and it receptor c-kit in the development of chronic pulmonary disease.

4. The signal transduction of chemokine and toll-like receptors on immune and non-immune cell populations.

5. The role of IL-25 for driving Th2 responses in chronic inflammation.