Granuloma formation, implications for the pathogenesis of vasculitis.
The pathogenesis of granulomatous inflammation is complex and involves a variety of mechanisms acting in concert to bring about an inflammatory lesion that is able to contain and destroy intracellular pathogens. While this process is crucial to host defense, it is also a two-edged sword in that excessive or inappropriate granulomatous inflammation results in considerable damage to normal tissue. In recent years, there has been significant progress in dissecting the immunologic events involved in granuloma formation and maintenance. A better understanding of these events will allow us to more precisely modulate the granulomatous inflammatory response to the benefit of patients with both infectious and autoimmune diseases.
Sneller
Michael C
MC
Laboratory of Immunoregulation, National Institute of Allergy, Immunology, and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. sneller@nih.gov
D013700:Giant Cell Arteritis / Q000276:immunology / Q000473:pathology; D006099:Granuloma / Q000276:immunology* / Q000503:physiopathology; D014890:Granulomatosis with Polyangiitis / Q000276:immunology / Q000473:pathology; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D013625:Takayasu Arteritis / Q000276:immunology / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014657:Vasculitis / Q000276:immunology* / Q000473:pathology*
D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12; D007371:Interferon-gamma