TAK1 restricts spontaneous NLRP3 activation and cell death to control myeloid proliferation
The NOD-like receptor (NLR)-P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling NLRP3 inflammasome activation are largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) is a centr...
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| Veröffentlicht in: | The Journal of experimental medicine Jg. 215; H. 4; S. 1023 |
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| Abstract | The NOD-like receptor (NLR)-P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling NLRP3 inflammasome activation are largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) is a central regulator of NLRP3 inflammasome activation and spontaneous cell death. Absence of TAK1 in macrophages induced spontaneous activation of the NLRP3 inflammasome without requiring toll-like receptor (TLR) priming and subsequent activating signals, suggesting a distinctive role for TAK1 in maintaining NLRP3 inflammasome homeostasis. Autocrine tumor necrosis factor (TNF) signaling in the absence of TAK1 induced spontaneous RIPK1-dependent NLRP3 inflammasome activation and cell death. We further showed that TAK1 suppressed homeostatic NF-κB and extracellular signal-related kinase (ERK) activation to limit spontaneous TNF production. Moreover, the spontaneous inflammation resulting from TAK1-deficient macrophages drives myeloid proliferation in mice, and was rescued by RIPK1 deficiency. Overall, these studies identify a critical role for TAK1 in maintaining NLRP3 inflammasome quiescence and preserving cellular homeostasis and survival. |
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| AbstractList | The NOD-like receptor (NLR)-P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling NLRP3 inflammasome activation are largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) is a central regulator of NLRP3 inflammasome activation and spontaneous cell death. Absence of TAK1 in macrophages induced spontaneous activation of the NLRP3 inflammasome without requiring toll-like receptor (TLR) priming and subsequent activating signals, suggesting a distinctive role for TAK1 in maintaining NLRP3 inflammasome homeostasis. Autocrine tumor necrosis factor (TNF) signaling in the absence of TAK1 induced spontaneous RIPK1-dependent NLRP3 inflammasome activation and cell death. We further showed that TAK1 suppressed homeostatic NF-κB and extracellular signal-related kinase (ERK) activation to limit spontaneous TNF production. Moreover, the spontaneous inflammation resulting from TAK1-deficient macrophages drives myeloid proliferation in mice, and was rescued by RIPK1 deficiency. Overall, these studies identify a critical role for TAK1 in maintaining NLRP3 inflammasome quiescence and preserving cellular homeostasis and survival. The NOD-like receptor (NLR)-P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling NLRP3 inflammasome activation are largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) is a central regulator of NLRP3 inflammasome activation and spontaneous cell death. Absence of TAK1 in macrophages induced spontaneous activation of the NLRP3 inflammasome without requiring toll-like receptor (TLR) priming and subsequent activating signals, suggesting a distinctive role for TAK1 in maintaining NLRP3 inflammasome homeostasis. Autocrine tumor necrosis factor (TNF) signaling in the absence of TAK1 induced spontaneous RIPK1-dependent NLRP3 inflammasome activation and cell death. We further showed that TAK1 suppressed homeostatic NF-κB and extracellular signal-related kinase (ERK) activation to limit spontaneous TNF production. Moreover, the spontaneous inflammation resulting from TAK1-deficient macrophages drives myeloid proliferation in mice, and was rescued by RIPK1 deficiency. Overall, these studies identify a critical role for TAK1 in maintaining NLRP3 inflammasome quiescence and preserving cellular homeostasis and survival.The NOD-like receptor (NLR)-P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling NLRP3 inflammasome activation are largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) is a central regulator of NLRP3 inflammasome activation and spontaneous cell death. Absence of TAK1 in macrophages induced spontaneous activation of the NLRP3 inflammasome without requiring toll-like receptor (TLR) priming and subsequent activating signals, suggesting a distinctive role for TAK1 in maintaining NLRP3 inflammasome homeostasis. Autocrine tumor necrosis factor (TNF) signaling in the absence of TAK1 induced spontaneous RIPK1-dependent NLRP3 inflammasome activation and cell death. We further showed that TAK1 suppressed homeostatic NF-κB and extracellular signal-related kinase (ERK) activation to limit spontaneous TNF production. Moreover, the spontaneous inflammation resulting from TAK1-deficient macrophages drives myeloid proliferation in mice, and was rescued by RIPK1 deficiency. Overall, these studies identify a critical role for TAK1 in maintaining NLRP3 inflammasome quiescence and preserving cellular homeostasis and survival. |
| Author | Mavuluri, Jayadev Kanneganti, Thirumala-Devi Malireddi, R K Subbarao Gurung, Prajwal Dasari, Tejasvi Krishna Klco, Jeffery M Chi, Hongbo |
| Author_xml | – sequence: 1 givenname: R K Subbarao surname: Malireddi fullname: Malireddi, R K Subbarao organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN – sequence: 2 givenname: Prajwal surname: Gurung fullname: Gurung, Prajwal organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN – sequence: 3 givenname: Jayadev surname: Mavuluri fullname: Mavuluri, Jayadev organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN – sequence: 4 givenname: Tejasvi Krishna surname: Dasari fullname: Dasari, Tejasvi Krishna organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN – sequence: 5 givenname: Jeffery M orcidid: 0000-0003-2961-6960 surname: Klco fullname: Klco, Jeffery M organization: Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN – sequence: 6 givenname: Hongbo orcidid: 0000-0002-9997-2496 surname: Chi fullname: Chi, Hongbo organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN – sequence: 7 givenname: Thirumala-Devi orcidid: 0000-0002-6395-6443 surname: Kanneganti fullname: Kanneganti, Thirumala-Devi email: Thirumala-Devi.Kanneganti@StJude.org organization: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN Thirumala-Devi.Kanneganti@StJude.org |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29500178$$D View this record in MEDLINE/PubMed |
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