Human IL-23-producing type 1 macrophages promote but IL-10-producing type 2 macrophages subvert immunity to (myco)bacteria.

By F. Verreck, T. de Boer, Dennis M. L. Langenberg, M. Hoeve, Matthijs Kramer, E. Vaisberg, R. Kastelein, A. Kolk, R. de Waal‐Malefyt, T. Ottenhoff. Proceedings of the National Academy of Sciences of the United States of America, 2004

1,040 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/b1437544108a4fc7dc6482abcb5f98987de58db5

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In Immunology

1. A. Mantovani
2. D. Cua
3. S. Gordon
4. F. Martínez
5. Shizuo Akira
6. O. Takeuchi
7. P. Italiani
8. D. Boraschi

Citations in the corpus

• Macrophage phenotypes in atherosclerosis (2014, background): “M1 macrophages contribute to an increased and sustained inflammatory response via the secretion of pro-inflammatory cytokines such as interleukin-6 (IL-6), IL1b, TNF (19), as well as IL-12 and IL-23 (20).”
• From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation (2014, background): “CSF-1 and GM-CSF are also involved in monocyte/macrophage functional differentiation programs: CSF-1 stimulation leads to a homeostatic or anti-inflammatory M2-like phenotype (25, 117, 118), whereas GM-CSF leads to an M1-like inflammatory phenotype (25, 117–119).”
• Efficient clearance of early apoptotic cells by human macrophages requires “M2c” polarization and MerTK induction (2012, background): “Because GM-CSF and M-CSF are known to drive M1 or M2 macrophage differentiation, respectively (33, 34), we studied the effects of other conventional M1 and M2 stimuli on terminally differentiated macrophages.”
• Role of Human Macrophage Polarization in Inflammation during Infectious Diseases (2018, background): “in order to recruit neutrophils, monocytes, and T lymphocytes in an anti‐inflammatory or regulatory response [23,24].”
• Glioma cancer stem cells induce immunosuppressive macrophages/microglia. (2010, methodology): “To evaluate the role of gCSCs on MF function, human monocytes were isolated from peripheral blood of normal donors and induced to differentiate into MFs in vitro.(47) Phenotypic markers indicated at least .”
• IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2–dependent mechanisms with implications for psoriasis pathogenesis (2006, background): “IL-23 is produced by dendritic cells and macrophages in response to bacteria, including Bordetella pertussis (17), Mycobacterium tuberculosis (18), Streptococcus pyogenes (19), and Klebsiella pneumoniae (20).”
• Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression1 (2006, result): “Macrophages were obtained by culturing monocytes (98% CD14 ϩ , 13% CD16 ϩ ) for 7 days in RPMI 1640 (Biochrom) supplemented with 20% FCS (HyClone) and 100 ng/ml M-CSF in FCS-coated dishes at a density of 1.5 ϫ 10 5 /cm 2 .”
• The encephalitogenicity of TH17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF (2011, positive): “Our data and those of others have demonstrated that GM-CSF induces IL-23 in APCs, which in turn induce GM-CSF expression by T H 17 cells, resulting in amplification of the inflammatory respons”
• The Jmjd3-Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection (2010, background): “Among growth factors, treatment of bone marrow cells with granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF) leads to generation of M1 and M2 cells, respectivel”