Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB

By C. Porta, M. Rimoldi, G. Raes, L. Brys, P. Ghezzi, D. Di Liberto, F. Dieli, S. Ghisletti, G. Natoli, P. De Baetselier and 2 more. Proceedings of the National Academy of Sciences of the United States of America, 2009

651 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/b360e8d295123ab17e6e5cde7d7e84575837bfd8

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Citations in the corpus

Alternative activation of macrophages: mechanism and functions. (2010, background): “Porta and colleagues have shown that tolerance and alternative activation (M2 polarization) are related processes mediated by p50 homodimers, which lack a transcription activation domain of members of the NF-kB pathway (Porta et al., 2009).”
Much More than M1 and M2 Macrophages, There are also CD169+ and TCR+ Macrophages (2015, methodology): “It has been shown that the NFκB p50 subunit, in the form of homodimers, has a regulatory activity essential for M2 polarization, both in vitro and in vivo (101).”
Transforming Grown Factor-β Signaling in Immunity and Cancer (2019, unknown): “Indeed, the acquisition of a M2 phenotype in TAMs correlates with inhibition of NF-κB activity (Porta et al., 2009).”
Macrophage plasticity and interaction with lymphocyte subsets: cancer as a paradigm (2010, background): “Endotoxin-tolerant macrophages have been found to express a set of molecules that overlap those expressed by alternatively activated (M2-polarized) macrophage”
Macrophages, innate immunity and cancer: balance, tolerance, and diversity. (2010, background): “A detailed analysis of the role of p50 NF-kB homodimer in macrophage functions revealed that its nuclear accumulation, both in TAM and LPStolerant macrophages, not only mediates a status of unresponsiveness (tolerance) toward pro-inflammatory signals, but also actually plays as key regulator of M2dr”
Macrophage Polarization in Inflammatory Diseases (2014, background): “A recent study has confirmed that the p50 subunit of NF-κB served as the key regulator of M2-driven LPS-tolerant state in this transformation [26] .”
Macrophage Polarization. (2017, background): “Increases IL-4Rα expression (same pathway as mediated by IL-10) IL12a IL12a Yes Indirect defects in TH1 responses (and hence IFN-γ production) Il12b Il12b Yes Indirect defects in TH1 responses (and hence IFN-γ production) Il23a Il23a Yes ND IL27 IL27 Yes ND Tnf Tnf Yes Required to suppress M2 macrop”
INTERLEUKIN-4- AND INTERLEUKIN-13-MEDIATED ALTERNATIVELY ACTIVATED MACROPHAGES: ROLES IN HOMEOSTASIS AND DISEASE (2013, unknown): “This type of signal integration is further apparent upon exposure to CAMpolarizing stimuli, as PPARγ expression in macrophages is suppressed upon LPS exposure (149); however, interestingly, macrophages induced to become LPS tolerant exhibit an AAM phenotype by a mechanism regulated by the p50 subuni”
Inflammation meets cancer, with NF-κB as the matchmaker (2011, background): “It has been shown that p50 inhibits NF-κB-driven M1 polarization, and p50-deficient mice have exacerbated M1-driven inflammation and a defective ability to mount allergy- and helminth-driven M2-polarized inflammatory reaction”
The polarization of immune cells in the tumour environment by TGFβ (2010, background): “Interestingly, the M2 phenotype of TAMs is mediated by the inhibitory nuclear factor-κB (NF-κB) subunit p50 and it is thought that the cytokine milieu of the tumour microenvironment is necessary to maintain the phenotyp”
Macrophage activation and polarization: nomenclature and experimental guidelines (2014, unknown): “…(1) removal of the stimulus, (2) enforcement of feedback and feed-forward signaling loops, including autocrine production of cytokines, and (3) epigenetic and/or developmental effects built into the life history of a macrophage (Ivashkiv, 2013; Lawrence and Natoli, 2011; Porta et al., 2009).”
IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses (2011, unknown): “Activation of the transcription factor NF-κB subunit p50 has been associated with the inhibition of M1-polarizing gene”
NF-κB, an Active Player in Human Cancers (2014, unknown): “Consistent with this idea, NF-κ B protein p50 has been shown to suppress M1-and induce M2-polarization of macrophage, thus favoring the immunosuppressive microenvironment (20).”