Regulation of Effector T Cell Migration within Inflamed Tissues
Fundamental to immune-mediated protection is the ability of leukocytes to survey barrier surfaces and quickly respond to infection or tissue damage. Signals from cytokines, chemokines and cells (immune and stromal) within the tissue provide critical cues for T cell migration at sites of inflammation, but the mechanics of T cell motility to these signals is poorly understood.
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Execution of CD4 Effector Function
The molecular control of CD4 differentiation into functionally distinct effector lineages has been extensively studied but the fate of the effector T cells once they leave the lymph node is less well understood. We are interested in how the inflammatory milieu at sites of infection and autoimmune attack may modify the effector function of CD4+ T cells.
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CD4 T Cell Motility in Inflamed Tissue
Cell migration is determined by the cell-intrinsic machinery for motility such as integrins, actin regulators and chemokine receptors and by the extrinsic composition of the extracellular matrix. The way in which effector CD4 T cells navigate through inflamed interstitial tissue at sites of infection is not well understood.
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Immune Regulation by Regulatory T Cells
Regulatory T cells (Tregs) play an important role in modulating immune response to self-antigens and infectious agents. Multiple regulatory mechanisms have been assigned to Tregs but how they modulate discrete immune functions has not been well defined. We are interested in determining how Tregs block cytokine production by CD4 T cells and how effector T cells may in turn modulate Treg function.
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