University of Cambridge > Talks.cam > Immunology in Pathology > Dr Yongliang Zhang: MKP5, a novel regulator of IRF3-type I IFNs, critically modulates host-pathogen interaction in influenza and other RNA virus infections.

Dr Yongliang Zhang: MKP5, a novel regulator of IRF3-type I IFNs, critically modulates host-pathogen interaction in influenza and other RNA virus infections.

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Host: Prof John Trowsdale (jt233@cam.ac.uk)

MAPK phosphatases (MKPs), also known as dual-specificity phosphatases (DUSPs), are known as important regulators in both innate and adaptive immune responses, mainly through their regulation of MAP kinase activation. Previously, we have shown that MKP5 , one of the MKP proteins, is important for T helper cell activation and effector function by targeting JNK .

Our recent investigation on this protein reveals a novel function of MKP5 in innate immune response to infection of RNA viruses including influenza virus, vesicular stomatitis virus and Sendai virus. The interferon regulatory factor 3 (IRF3) is known as the master regulator of type I interferons (IFNs) which are essential for host defence against viral infection. We found that the expression MKP5 induced by virus infection inactivates IRF3 , thereby inhibiting type I IFN response.

Therefore, the induction of MKP5 expression could be part of the viral immune evasion strategies to escape the type I IFN response. At the same time, MKP5 could be a strategy of the host to regulate the intensity of antiviral immune response to avoid uncontrolled immunopathology.

This talk is part of the Immunology in Pathology series.

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