Danielle Burger

Biography

Monocyte/Macrophage Activation in Chronic/Sterile Inflammation: regulation of cytokine homeostatis Background: The inflammatory response aims at protecting the organism by clearing out the initial cause of cell injury (e.g., microorganisms or toxins) and the consequences of such injury (e.g., necrotic cells and tissues), and in turn at initiating mechanisms designed at repairing surrounding damaged tissues. Inflammation has to be tightly controlled in time and space to avoid detrimental developments such as those seen in sepsis and chronic inflammatory diseases including rheumatoid arthritis (RA) and multiple sclerosis (MS). Monocytes/macrophages play critical parts in non-septic T cell-mediated chronic inflammatory diseases as exemplified by multiple sclerosis (MS) and rheumatoid arthritis (RA). Monocytes/macrophages are the major producers of cytokines at inflammatory sites in both chronic/sterile and acute/infectious inflammation. Cell-cell contact with stimulated T lymphocytes is now considered a major pathway triggering monocytes/macrophages to produce inflammatory mediators in the absence of infectious agents. This mechanism is likely to be relevant to chronic inflammatory diseases, particularly in the perivascular region of local sites of inflammation where T lymphocytes and monocytes/macrophages are in close proximity. This is also the region where apolipoprotein A-I - a specific inhibitor of contact-mediated activation of monocytes - accumulates upon active inflammation.

Research Interest

Nephrology