Lamkanfi Unit - NOD-like Receptor and Inflammasome Laboratory

Research field: Pathogen sensing and inflammation

Group leader: Prof. Dr. Mohamed Lamkanfi

Tel:  +32 9 33 13730 -  Fax:+32 9 221 76 73
E-mail:
Mohamed.Lamkanfi.spam.detractor@irc.vib-UGentspam.corruptor.be

Research topic

The major research interest of the NOD-like Receptor and Inflammasome Laboratory is how NOD-like receptors (NLRs) and inflammasomes modulate immune responses. NLRs represent a family of intracellular receptors by which immune cells detect and mount immune responses against invading pathogens. Mutations in NLR genes are associated with auto-inflammatory and -immune disorders, including Crohn’s disease, arthritis, diabetes, period fever syndromes, asthma, atopic eczema, Blau syndrome and vitiligo. While some NLRs regulate NF-κB signaling and interferon responses, another subset of the 22 NLR proteins encoded in the human genome is responsible for production of interleukin (IL)-1ß and IL-18 through activation of the cysteine proteases caspases-1 and -11 in protein complexes termed ‘inflammasomes’.

Area of expertise

  • NOD-like receptors
  • Inflammasomes
  • Pyroptosis
  • Innate immunity
  • Inflammation

Technology transfer potential

  • Assays and therapeutic targets in inflammation and autoimmunity
  • Mouse models of inflammasome-driven diseases

 

    Selected publications

    1. Matusiak M., et al. Flagellin-induced NLRC4 phosphorylation primes the inflammasome for activation by NAIP5.
      Proceedings of the National Academy of Sciences USA. 112(5):1541-1546, 2015
    2. Vande Walle L., et al. Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis.
      Nature 512(7512):69-73, 2014
    3. Lamkanfi M., Dixit V.M. Mechanisms and Functions of Inflammasomes.
      Cell 157(5):1013-1022. 2014.
    4. Demon D., et al. Caspase-11 protects against colitis independently of inflammasome-mediated cytokine production.
      Mucosal Immunology  7(6):1480-91, 2014
    5. Van Opdenbosch N., et al. ASC-driven caspase-1 autoproteolysis and speck formation are dispensable for Nlrp1b inflammasome activation.
      Nature Communications 5:3209, 2014

     


    Macrophage undergoing pyroptotic cell death

     

     


    Intestinal inflammation in caspase-11-deficient mice

     

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