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• W2102768377 abstract "IL-6 can mediate proinflammatory effects, and IL-6 receptor (IL-6R) blockade as a treatment for inflammatory diseases has entered clinical practice. However, opposing effects of IL-6 have been observed in models of GN. Although IL-6 is proinflammatory in murine lupus nephritis, protective effects have been observed for IL-6 in the nephrotoxic nephritis (NTN) model of acute crescentic GN. In light of the potential dangers of IL-6-directed treatment, we studied the mechanisms underlying the contradictory findings in GN. IL-6 can signal through the membrane-bound IL-6R, which is expressed only on hepatocytes and certain leukocytes (classic), or through the soluble IL-6R, which binds the ubiquitously expressed gp130 (alternative). Preemptive treatment of mice with anti-IL-6R or anti-IL-6 worsened NTN, whereas selective blockade of alternative IL-6 signaling by the fusion protein sgp130Fc did not. FACS analysis of mouse spleen cells revealed proinflammatory macrophages express the highest levels of IL-6Rα, and in vitro treatment with IL-6 blocked macrophage proliferation. Furthermore, proinflammatory macrophages were expanded during inflammation in IL-6(-/-) mice. Late application of anti-IL-6 after establishment of adaptive nephritogenic immunity was sufficient to aggravate NTN within 2.5 days, a period when macrophages are active. Finally, NTN was aggravated in mice with macrophage-specific impairment of IL-6 classic signaling, coincident with enhanced macrophage proliferation and accumulation in the kidney. Our data thus reveal a novel mechanism in which IL-6-mediated dampening of macrophage activation protects tissues from overshooting immune responses. This finding has important implications for potential IL-6-directed therapies and supports the careful choice of recipient patients and timing." @default.
• W2102768377 created "2016-06-24" @default.
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• W2102768377 date "2015-07-01" @default.
• W2102768377 modified "2023-10-12" @default.
• W2102768377 title "Inflammation-Induced IL-6 Functions as a Natural Brake on Macrophages and Limits GN" @default.
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• W2102768377 doi "https://doi.org/10.1681/asn.2014060620" @default.
• W2102768377 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4483592" @default.
• W2102768377 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25655068" @default.
• W2102768377 hasPublicationYear "2015" @default.
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