The Pseudokinase MLKL and the Kinase RIPK3 Have Distinct Roles in Autoimmune Disease Caused by Loss of Death-Receptor-Induced Apoptosis

The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL within the whole animal has not yet been established. Here, we have shown that MLKL deficiency rescued the embryonic lethality caused by loss...

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Published inImmunity (Cambridge, Mass.) Vol. 45; no. 3; pp. 513 - 526
Main Authors Alvarez-Diaz, Silvia, Dillon, Christopher P., Lalaoui, Najoua, Tanzer, Maria C., Rodriguez, Diego A., Lin, Ann, Lebois, Marion, Hakem, Razq, Josefsson, Emma C., O’Reilly, Lorraine A., Silke, John, Alexander, Warren S., Green, Douglas R., Strasser, Andreas
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 20.09.2016
Elsevier Limited
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Abstract The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL within the whole animal has not yet been established. Here, we have shown that MLKL deficiency rescued the embryonic lethality caused by loss of Caspase-8 or FADD. Casp8−/−Mlkl−/− and Fadd−/−Mlkl−/− mice were viable and fertile but rapidly developed severe lymphadenopathy, systemic autoimmune disease, and thrombocytopenia. These morbidities occurred more rapidly and with increased severity in Casp8−/−Mlkl−/− and Fadd−/−Mlkl−/− mice compared to Casp8−/−Ripk3−/− or Fadd−/−Ripk3−/− mice, respectively. These results demonstrate that MLKL is an essential effector of aberrant necroptosis in embryos caused by loss of Caspase-8 or FADD. Furthermore, they suggest that RIPK3 and/or MLKL may exert functions independently of necroptosis. It appears that non-necroptotic functions of RIPK3 contribute to the lymphadenopathy, autoimmunity, and excess cytokine production that occur when FADD or Caspase-8-mediated apoptosis is abrogated. •MLKL is an essential effector of necroptosis in vivo•RIPK3 exacerbates the development and progression of ALPS-like disease•RIPK3 and maybe MLKL exert additional functions beyond inducing cell death Necroptosis is a form of regulated cell death implicated in several pathologies. MLKL was shown to be critical for necroptosis in vitro. Alvarez-Diaz et al. demonstrate that MLKL, like RIPK3, is essential for necroptosis in vivo and reveal that RIPK3 also has a role beyond cell death in promoting lymphadenopathy and autoimmune disease.
AbstractList The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL within the whole animal has not yet been established. Here, we have shown that MLKL deficiency rescued the embryonic lethality caused by loss of Caspase-8 or FADD. Casp8(-/-)Mlkl(-/-) and Fadd(-/-)Mlkl(-/-) mice were viable and fertile but rapidly developed severe lymphadenopathy, systemic autoimmune disease, and thrombocytopenia. These morbidities occurred more rapidly and with increased severity in Casp8(-/-)Mlkl(-/-) and Fadd(-/-)Mlkl(-/-) mice compared to Casp8(-/-)Ripk3(-/-) or Fadd(-/-)Ripk3(-/-) mice, respectively. These results demonstrate that MLKL is an essential effector of aberrant necroptosis in embryos caused by loss of Caspase-8 or FADD. Furthermore, they suggest that RIPK3 and/or MLKL may exert functions independently of necroptosis. It appears that non-necroptotic functions of RIPK3 contribute to the lymphadenopathy, autoimmunity, and excess cytokine production that occur when FADD or Caspase-8-mediated apoptosis is abrogated.
The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL within the whole animal has not yet been established. Here, we have shown that MLKL deficiency rescued the embryonic lethality caused by loss of Caspase-8 or FADD. Casp8-/-Mlkl-/- and Fadd-/-Mlkl-/- mice were viable and fertile but rapidly developed severe lymphadenopathy, systemic autoimmune disease, and thrombocytopenia. These morbidities occurred more rapidly and with increased severity in Casp8-/-Mlkl-/- and Fadd-/-Mlkl-/- mice compared to Casp8-/-Ripk3-/- or Fadd-/-Ripk3-/- mice, respectively. These results demonstrate that MLKL is an essential effector of aberrant necroptosis in embryos caused by loss of Caspase-8 or FADD. Furthermore, they suggest that RIPK3 and/or MLKL may exert functions independently of necroptosis. It appears that non-necroptotic functions of RIPK3 contribute to the lymphadenopathy, autoimmunity, and excess cytokine production that occur when FADD or Caspase-8-mediated apoptosis is abrogated.
The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL within the whole animal has not yet been established. Here, we have shown that MLKL deficiency rescued the embryonic lethality caused by loss of Caspase-8 or FADD. Casp8 −/− Mlkl −/− and Fadd −/− Mlkl −/− mice were viable and fertile but rapidly developed severe lymphadenopathy, systemic autoimmune disease and thrombocytopenia. These morbidities occurred more rapidly and with increased severity in Casp8 −/− Mlkl −/− and Fadd −/− Mlkl −/− mice compared to Casp8 −/− Ripk3 −/− or Fadd −/− Ripk3 −/− mice, respectively. These results demonstrate that MLKL is an essential effector of necroptosis in embryos caused by loss of Caspase-8 or FADD. Furthermore, they suggest that RIPK3 and/or MLKL may exert functions independently of necroptosis. It appears that non-necroptotic functions of RIPK3 contribute to the lymphadenopathy, autoimmunity and excess cytokine production that occur when FADD or caspase-8 mediated apoptosis is abrogated.
The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL within the whole animal has not yet been established. Here, we have shown that MLKL deficiency rescued the embryonic lethality caused by loss of Caspase-8 or FADD. Casp8−/−Mlkl−/− and Fadd−/−Mlkl−/− mice were viable and fertile but rapidly developed severe lymphadenopathy, systemic autoimmune disease, and thrombocytopenia. These morbidities occurred more rapidly and with increased severity in Casp8−/−Mlkl−/− and Fadd−/−Mlkl−/− mice compared to Casp8−/−Ripk3−/− or Fadd−/−Ripk3−/− mice, respectively. These results demonstrate that MLKL is an essential effector of aberrant necroptosis in embryos caused by loss of Caspase-8 or FADD. Furthermore, they suggest that RIPK3 and/or MLKL may exert functions independently of necroptosis. It appears that non-necroptotic functions of RIPK3 contribute to the lymphadenopathy, autoimmunity, and excess cytokine production that occur when FADD or Caspase-8-mediated apoptosis is abrogated. •MLKL is an essential effector of necroptosis in vivo•RIPK3 exacerbates the development and progression of ALPS-like disease•RIPK3 and maybe MLKL exert additional functions beyond inducing cell death Necroptosis is a form of regulated cell death implicated in several pathologies. MLKL was shown to be critical for necroptosis in vitro. Alvarez-Diaz et al. demonstrate that MLKL, like RIPK3, is essential for necroptosis in vivo and reveal that RIPK3 also has a role beyond cell death in promoting lymphadenopathy and autoimmune disease.
The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL within the whole animal has not yet been established. Here, we have shown that MLKL deficiency rescued the embryonic lethality caused by loss of Caspase-8 or FADD.Casp8-/-Mlkl-/-andFadd-/-Mlkl-/-mice were viable and fertile but rapidly developed severe lymphadenopathy, systemic autoimmune disease, and thrombocytopenia. These morbidities occurred more rapidly and with increased severity inCasp8-/-Mlkl-/-andFadd-/-Mlkl-/-mice compared toCasp8-/-Ripk3-/-orFadd-/-Ripk3-/-mice, respectively. These results demonstrate that MLKL is an essential effector of aberrant necroptosis in embryos caused by loss of Caspase-8 or FADD. Furthermore, they suggest that RIPK3 and/or MLKL may exert functions independently of necroptosis. It appears that non-necroptotic functions of RIPK3 contribute to the lymphadenopathy, autoimmunity, and excess cytokine production that occur when FADD or Caspase-8-mediated apoptosis is abrogated.
Author Strasser, Andreas
Tanzer, Maria C.
Josefsson, Emma C.
Rodriguez, Diego A.
Lin, Ann
Alexander, Warren S.
Hakem, Razq
O’Reilly, Lorraine A.
Dillon, Christopher P.
Lebois, Marion
Green, Douglas R.
Lalaoui, Najoua
Silke, John
Alvarez-Diaz, Silvia
AuthorAffiliation 1 The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
2 Department of Medical Biology, University of Melbourne, Parkville, Victoria 3050, Australia
4 Ontario Cancer Institute, University Health Network, and Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada M5G 2M9
3 Department of Immunology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA
AuthorAffiliation_xml – name: 4 Ontario Cancer Institute, University Health Network, and Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada M5G 2M9
– name: 1 The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
– name: 3 Department of Immunology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA
– name: 2 Department of Medical Biology, University of Melbourne, Parkville, Victoria 3050, Australia
Author_xml – sequence: 1
  givenname: Silvia
  surname: Alvarez-Diaz
  fullname: Alvarez-Diaz, Silvia
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  givenname: Christopher P.
  surname: Dillon
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  givenname: Najoua
  surname: Lalaoui
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  organization: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
– sequence: 4
  givenname: Maria C.
  surname: Tanzer
  fullname: Tanzer, Maria C.
  organization: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
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  givenname: Diego A.
  surname: Rodriguez
  fullname: Rodriguez, Diego A.
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  organization: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
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  surname: Lebois
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  organization: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
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  fullname: Hakem, Razq
  organization: Ontario Cancer Institute, University Health Network, and Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada
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  givenname: Emma C.
  surname: Josefsson
  fullname: Josefsson, Emma C.
  organization: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
– sequence: 10
  givenname: Lorraine A.
  surname: O’Reilly
  fullname: O’Reilly, Lorraine A.
  organization: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
– sequence: 11
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  surname: Silke
  fullname: Silke, John
  organization: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
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  givenname: Warren S.
  surname: Alexander
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  email: strasser@wehi.edu.au
  organization: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27523270$$D View this record in MEDLINE/PubMed
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Douglas R. Green, 262 Danny Thomas Place, Memphis, TN 38105, USA, douglas.greem@stjude.org
Warren S Alexander, The Walter and Eliza Hall Institute, 1G Royal Parade, Parkville, VIC 3052, Australia, alexandw@wehi.edu.au
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Snippet The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL...
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SubjectTerms Animals
Apoptosis
Apoptosis - physiology
Autoimmune diseases
Autoimmune Diseases - metabolism
Caspase 8 - metabolism
Cell Death - physiology
Cloning
Evacuations & rescues
Fas-Associated Death Domain Protein - metabolism
Gangrene
Immunoglobulins
Kinases
Ligands
Lymphocytes
Medical research
Mice
Mice, Inbred C57BL
Necrosis - metabolism
Protein Kinases - metabolism
Receptor-Interacting Protein Serine-Threonine Kinases - metabolism
Statistical analysis
Tumor necrosis factor-TNF
Title The Pseudokinase MLKL and the Kinase RIPK3 Have Distinct Roles in Autoimmune Disease Caused by Loss of Death-Receptor-Induced Apoptosis
URI https://dx.doi.org/10.1016/j.immuni.2016.07.016
https://www.ncbi.nlm.nih.gov/pubmed/27523270
https://www.proquest.com/docview/1822649643
https://search.proquest.com/docview/1823033606
https://search.proquest.com/docview/1827905709
https://pubmed.ncbi.nlm.nih.gov/PMC5040700
Volume 45
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