M G Netea


Affiliation: Radboud University Nijmegen Medical Centre
Country: The Netherlands


  1. request reprint
    Netea M, Ferwerda G, de Jong D, Girardin S, Kullberg B, van der Meer J. NOD2 3020insC mutation and the pathogenesis of Crohn's disease: impaired IL-1beta production points to a loss-of-function phenotype. Neth J Med. 2005;63:305-8 pubmed
    ..This sustains the hypothesis that the 3020insC mutation in the human NOD2 gene leads to a loss-of-function phenotype. ..
  2. Netea M, Nold Petry C, Nold M, Joosten L, Opitz B, van der Meer J, et al. Differential requirement for the activation of the inflammasome for processing and release of IL-1beta in monocytes and macrophages. Blood. 2009;113:2324-35 pubmed publisher
    ..We conclude that IL-1beta production is differentially regulated in monocytes and macrophages, and this reflects their separate functions in host defense and inflammation. ..
  3. Bai X, Kinney W, Su W, Bai A, Ovrutsky A, Honda J, et al. Caspase-3-independent apoptotic pathways contribute to interleukin-32γ-mediated control of Mycobacterium tuberculosis infection in THP-1 cells. BMC Microbiol. 2015;15:39 pubmed publisher
    ..The anti-MTB effects of IL-32γ are mediated through classical caspase-3-dependent apoptosis as well as caspase-3-independent apoptosis. ..
  4. Alexis A, Carrer D, Droggiti D, Louis K, Pistiki A, Netea M, et al. Immune responses in relation to the type and time of thermal injury: an experimental study. Injury. 2015;46:227-32 pubmed publisher
    ..This study was based on an experimental murine model. There is a unique response for each type of injury depending on the temperature of the thermal source and the exposure time. ..
  5. request reprint
    Netea M, Ferwerda G, de Jong D, Jansen T, Jacobs L, Kramer M, et al. Nucleotide-binding oligomerization domain-2 modulates specific TLR pathways for the induction of cytokine release. J Immunol. 2005;174:6518-23 pubmed
    ..Thus, interaction between NOD2 and specific TLR pathways may represent an important modulatory mechanism of innate immune responses. ..
  6. Kleinnijenhuis J, Joosten L, van de Veerdonk F, Savage N, van Crevel R, Kullberg B, et al. Transcriptional and inflammasome-mediated pathways for the induction of IL-1beta production by Mycobacterium tuberculosis. Eur J Immunol. 2009;39:1914-22 pubmed publisher
    ..In conclusion, we have dissected the molecular mechanisms responsible for IL-1beta production by M. tuberculosis, and that may contribute to a deeper knowledge of the mechanisms of cell activation by M. tuberculosis. ..
  7. Smeekens S, Gresnigt M, Becker K, Cheng S, Netea S, Jacobs L, et al. An anti-inflammatory property of Candida albicans β-glucan: Induction of high levels of interleukin-1 receptor antagonist via a Dectin-1/CR3 independent mechanism. Cytokine. 2015;71:215-22 pubmed publisher
    ..These data strongly argue for the existence of an unknown β-glucan receptor that specifically induces an Akt/PI3K-dependent anti-inflammatory IL-1Ra response upon recognition of C. albicans. ..
  8. Netea M, Simon A, van de Veerdonk F, Kullberg B, Van der Meer J, Joosten L. IL-1beta processing in host defense: beyond the inflammasomes. PLoS Pathog. 2010;6:e1000661 pubmed publisher
    ..In conclusion, IL-1beta/IL-18 processing during infection is a complex process in which the inflammasomes are only one of several activation mechanisms. ..
  9. Netea M, Marodi L. Innate immune mechanisms for recognition and uptake of Candida species. Trends Immunol. 2010;31:346-53 pubmed publisher
    ..In addition, the consequence of genetic defects in dectin-1 and dectin-1-mediated signalling and the role of Th17-dependent mechanisms for the mucosal antifungal defence are discussed. ..

More Information


  1. Oosting M, Buffen K, Malireddi S, Sturm P, Verschueren I, Koenders M, et al. Murine Borrelia arthritis is highly dependent on ASC and caspase-1, but independent of NLRP3. Arthritis Res Ther. 2012;14:R247 pubmed publisher
    ..Based on present results indicating that IL-1 is one of the major mediators in Lyme arthritis, there is a rationale to propose that neutralizing IL-1 activity may also have beneficial effects in chronic Lyme arthritis. ..
  2. Plantinga T, Fransen J, Takahashi N, Stienstra R, van Riel P, van den Berg W, et al. Functional consequences of DECTIN-1 early stop codon polymorphism Y238X in rheumatoid arthritis. Arthritis Res Ther. 2010;12:R26 pubmed publisher
  3. request reprint
    Netea M, van de Veerdonk F, Verschueren I, Van der Meer J, Kullberg B. Role of TLR1 and TLR6 in the host defense against disseminated candidiasis. FEMS Immunol Med Microbiol. 2008;52:118-23 pubmed
    ..In conclusion, TLR6 is involved in the recognition of C. albicans and modulates the Th1/Th2 cytokine balance, but this results in a mild phenotype with a normal susceptibility of TLR6-/- mice to Candida infection. ..
  4. request reprint
    Netea M, Joosten L, Lewis E, Jensen D, Voshol P, Kullberg B, et al. Deficiency of interleukin-18 in mice leads to hyperphagia, obesity and insulin resistance. Nat Med. 2006;12:650-6 pubmed
    ..In addition, rIL-18 reversed hyperglycemia in Il18-/- mice through activation of STAT3 phosphorylation. These findings indicate a new role of IL-18 in the homeostasis of energy intake and insulin sensitivity. ..
  5. request reprint
    Netea M, Kullberg B, de Jong D, Franke B, Sprong T, Naber T, et al. NOD2 mediates anti-inflammatory signals induced by TLR2 ligands: implications for Crohn's disease. Eur J Immunol. 2004;34:2052-9 pubmed
    ..In conclusion, defective NOD2 function results in a pro-inflammatory cytokine bias after stimulation of mononuclear cells with TLR2 stimuli, and this could contribute to the overwhelming inflammation seen in Crohn's disease. ..
  6. request reprint
    Netea M, Kullberg B, Jacobs L, Verver Jansen T, van der Ven Jongekrijg J, Galama J, et al. Chlamydia pneumoniae stimulates IFN-gamma synthesis through MyD88-dependent, TLR2- and TLR4-independent induction of IL-18 release. J Immunol. 2004;173:1477-82 pubmed
    ..Most interestingly, C. pneumoniae is also a potent inducer of IL-18 production through pathways independent of TLR2 and TLR4. ..
  7. Netea M, Azam T, Lewis E, Joosten L, Wang M, Langenberg D, et al. Mycobacterium tuberculosis induces interleukin-32 production through a caspase- 1/IL-18/interferon-gamma-dependent mechanism. PLoS Med. 2006;3:e277 pubmed
    ..tuberculosis-induced IL-18 via caspase-1. In conclusion, IL-32 is a cell-associated proinflammatory cytokine, which is specifically stimulated by mycobacteria through a caspase-1- and IL-18-dependent production of IFNgamma. ..