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Cecilia Garlanda
Researcher at Humanitas University
Publications - 245
Citations - 28805
Cecilia Garlanda is an academic researcher from Humanitas University. The author has contributed to research in topics: Innate immune system & PTX3. The author has an hindex of 76, co-authored 227 publications receiving 24651 citations. Previous affiliations of Cecilia Garlanda include University of Brescia & Mario Negri Institute for Pharmacological Research.
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Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability.
TL;DR: This work surmises that CRI represents the seventh hallmark of cancer, and suggests that an additional mechanism involved in cancer-related inflammation (CRI) is induction of genetic instability by inflammatory mediators, leading to accumulation of random genetic alterations in cancer cells.
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The Interleukin-1 Family: Back to the Future
TL;DR: The key properties of IL-1 family members are reviewed, with emphasis on pathways of negative regulation and orchestration of innate and adaptive immunity.
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Central role for G protein-coupled phosphoinositide 3-kinase γ in inflammation
Emilio Hirsch,Vladimir L. Katanaev,Cecilia Garlanda,Ornella Azzolino,Luciano Pirola,Lorenzo Silengo,Silvano Sozzani,Alberto Mantovani,Alberto Mantovani,Fiorella Altruda,Matthias P. Wymann +10 more
TL;DR: Results demonstrate that PI3Kγ is a crucial signaling molecule required for macrophage accumulation in inflammation and shows reduced migration toward a wide range of chemotactic stimuli and a severely defective accumulation in a septic peritonitis model.
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Pentraxins at the crossroads between innate immunity, inflammation, matrix deposition, and female fertility.
TL;DR: The prototypic long pentraxin PTX3 is a multifunctional soluble pattern recognition receptor at the crossroads between innate immunity, inflammation, matrix deposition, and female fertility.
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AHR drives the development of gut ILC22 cells and postnatal lymphoid tissues via pathways dependent on and independent of Notch
Jacob S. Lee,Marina Cella,Keely G. McDonald,Cecilia Garlanda,Gregory D. Kennedy,Manabu Nukaya,Alberto Mantovani,Raphael Kopan,Christopher A. Bradfield,Rodney D. Newberry,Marco Colonna +10 more
TL;DR: It is found that Ahr−/− mice had a considerable deficit in ILC22 cells that resulted in less secretion of IL-22 and inadequate protection against intestinal bacterial infection.