ArticleEuropean journal of immunology2025
Fever-Induced Heat Shock Protein-70 Regulates Macrophage IL-1β and IL-10 Secretion During Mycobacterium tuberculosis Infection.
Article in European journal of immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The cycle of infectious fever - how it affects bacterial infections.Frontiers in cellular and infection microbiology · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Fever is a common clinical symptom in patients with tuberculosis (TB). During fever, heat-shock proteins (HSPs), such as HSP70, are expressed, which are molecular chaperones regulating protein folding and may also have immunomodulatory properties. How fever modulates immune responses during TB and by which mechanisms is unknown. In this study, we investigated the effects of fever, and specifically the role of HSP70, on Mycobacterium tuberculosis (Mtb)-induced macrophage inflammatory responses. Human monocyte-derived macrophages (MDM) were infected with Mtb at 37°C or 40°C to mimic febrile conditions. Fever suppresses Mtb-induced IL-1β and IL-10 gene expression and secretion from MDM, but enhances Mtb-induced HSP70 secretion and intracellular accumulation in MDM. Extracellular HSP70 and HSP70-expressing macrophages are abundant in granulomas in TB patient biopsies. HSP70 antagonism decreases Mtb-induced IL-1β secretion during febrile conditions but has no significant effect on IL-10 secretion. Pretreatment of MDM with recombinant HSP70 significantly increases Mtb-induced IL-1β at 37°C. Finally, extracellular HSP70 negatively regulates further HSP70 secretion from MDM during Mtb infection. Overall, fever and subsequent HSP70 expression modulates proinflammatory innate immune response in TB, which may have implications for the development of host-directed therapies.
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