DUCHENE MEGENS LAB - MOLECULAR INFLAMMATION

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  • The main objective of our research is to uncover novel molecular mechanisms that control inflammation and immune responses.



    • Inflammation is a natural immune response triggered by harmful stimuli, such as infections or injuries. Its primary function is to protect the body against potential threats and to promote the healing of damaged tissue. Nevertheless, when inflammation is dysregulated and becomes chronic, it can contribute to the pathogenesis of many diseases. Inflammation is a complex mechanism involving the tightly orchestrated action of multiple inflammatory molecules.
    • Our research focuses on studying the chemokine system, a key player in regulating inflammation and immune responses.

    • During the inflammatory response, chemokines govern the recruitment of circulating leukocytes and their migration to the inflamed sites. The effects of chemokines are mediated by G-protein coupled receptors (GPCRs), which are expressed in a wide range of immune cell types. Besides these "conventional" receptors (CCRs and CXCRs), chemokines also bind to atypical chemokine receptors (ACKRs), which control the availability of chemokines within tissues and thus influence immune cell behavior. The experimental work in our lab mainly focuses on the biology of ACKRs.

    LATEST NEWS FROM THE LAB

    Knocking Out Assumptions: Hidden Challenges in Transgenic Mouse Models

    17 Oct 2024 | News | Publication

    JLB 2024 ➤ IPEK scientists from the Duchene Lab have published critical findings on the limitations of genetic research using knockout mice.

    IPEK at Chemokines Gordon Research Conference 

    7 Jun 2024 | News | Award | Conference

    CONFERENCE HIGHLIGHT ➤ IPEK scientists from the Duchene Megens Lab participated in the Gordon Research Conference on Chemotactic Cytokines held in Portland, Maine, United States.

    How antibodies get it wrong

    CELL STEM CELL 2022 ➤  IPEK scientists alert to the wrong use of antibodies in scientific publications. In their recent work, they refute a specific study on localization of immune receptor ACKR1.