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Cancers 2019, 11(3), 298; https://doi.org/10.3390/cancers11030298

Macrophage Origin, Metabolic Reprogramming and IL-1β Signaling: Promises and Pitfalls in Lung Cancer

1
Institut National de la Santé et de la Recherche Médicale (Inserm) U1065, Université Côte d’Azur, Centre Méditerranéen de Médecine Moléculaire (C3M), Atip-Avenir, Fédération Hospitalo-Universitaire (FHU) Oncoage, 06204 Nice, France
2
Institut National de la Santé et de la Recherche Médicale (Inserm) UMR_S 1166, Sorbonnes Universités, Hôpital de la Pitié Salpêtrière, 75013 Paris, France
*
Author to whom correspondence should be addressed.
Received: 28 January 2019 / Revised: 21 February 2019 / Accepted: 26 February 2019 / Published: 2 March 2019
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Abstract

Macrophages are tissue-resident cells that act as immune sentinels to maintain tissue integrity, preserve self-tolerance and protect against invading pathogens. Lung macrophages within the distal airways face around 8000–9000 L of air every day and for that reason are continuously exposed to a variety of inhaled particles, allergens or airborne microbes. Chronic exposure to irritant particles can prime macrophages to mediate a smoldering inflammatory response creating a mutagenic environment and favoring cancer initiation. Tumor-associated macrophages (TAMs) represent the majority of the tumor stroma and maintain intricate interactions with malignant cells within the tumor microenvironment (TME) largely influencing the outcome of cancer growth and metastasis. A number of macrophage-centered approaches have been investigated as potential cancer therapy and include strategies to limit their infiltration or exploit their antitumor effector functions. Recently, strategies aimed at targeting IL-1β signaling pathway using a blocking antibody have unexpectedly shown great promise on incident lung cancer. Here, we review the current understanding of the bridge between TAM metabolism, IL-1β signaling, and effector functions in lung adenocarcinoma and address the challenges to successfully incorporating these pathways into current anticancer regimens. View Full-Text
Keywords: lung adenocarcinoma; macrophage; immunotherapy; interleukin-1β and immunometabolism lung adenocarcinoma; macrophage; immunotherapy; interleukin-1β and immunometabolism
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Guilbaud, E.; Gautier, E.L.; Yvan-Charvet, L. Macrophage Origin, Metabolic Reprogramming and IL-1β Signaling: Promises and Pitfalls in Lung Cancer. Cancers 2019, 11, 298.

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