Foamy macrophages and the progression of the human TB granuloma
By D. Russell, P. Cardona, Mi‐jeong Kim, Sophie Allain, F. Altare. Nature Immunology, 2009
809 citations recorded by the source corpus.
The progression of tuberculosis from a latent, subclinical infection to active disease that culminates in the transmission of infectious bacilli is determined locally at the level of the granuloma. This progression takes place even in the face of a robust immune response that, although it contains infection, is unable to eliminate the bacterium. The factors or environmental conditions that influence this progression remain to be determined. Recent advances have indicated that pathogen-induced dysregulation of host lipid synthesis and sequestration serves a critical role in this transition. The foamy macrophage seems to be a key participant in both sustaining persistent bacteria and contributing to the tissue pathology that leads to cavitation and the release of infectious bacilli.
Subfields: Epidemiology, Infectious Diseases, Surgery
View Paper: https://www.semanticscholar.org/paper/e04edc6da3663c8f2ca68132b9157e36a8976f1d
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Citations in the corpus
- The immune response in tuberculosis. (2013, background): “Human TB granulomas are composed of a central mass of infected macrophages, stimulated macrophages that have differentiated into multinucleated giant cells, epithelioid cells and foamy macrophages loaded with lipid droplets, and neutrophils (101).”
- Differential Macrophage Programming in the Tumor Microenvironment (2012, neutral): “In this context, tissue-resident macrophages assist with combating infection [1, 2], resolving acute inflammation [3], and in regulating metabolic response to tissue stress [4, 5].”