【摘 要】
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The innate immune system is critical for clearing infection,and is tightly regulated to avert excessive tissue damage.Nod1/2-Rip2 signaling,which is essential f
【机 构】
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Key Laboratory of Infection and Immunity of CAS, Institute of Biophysics, Chinese Academy of Science
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The innate immune system is critical for clearing infection,and is tightly regulated to avert excessive tissue damage.Nod1/2-Rip2 signaling,which is essential for initiating the innate immune response to bacterial infection and ER stress,is subject to many regulatory mechanisms.In this study,we found that LRRK2,encoded by a gene implicated in Crohn’s disease,leprosy and familial Parkinson’s disease,modulates the strength of Nod1/2-Rip2 signaling by enhancing Rip2 phosphorylation.LRRK2 deficiency markedly reduces cytokine production in macrophages upon Nod2 activation by muramyl dipeptide (MDP),Nod1 activation by D-gamma-Glu-meso-diaminopimelic acid (iE-DAP) or ER stress.Our biochemical study shows that the presence of LRRK2 is necessary for optimal phosphorylation of Rip2 upon Nod2 activation.Therefore,this study reveals that LRRK2 is a new positive regulator of Rip2 and promotes inflammatory cytokine induction through the Nod1/2-Rip2 pathway.
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