M G Netea

Summary

Affiliation: Radboud University Nijmegen Medical Centre
Country: The Netherlands

Publications

  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. ..

Detail Information

Publications7

  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. ..