Role for nuclear interleukin-37 in the suppression of innate immunity
The IL-1 family member IL-37 broadly suppresses innate inflammation and acquired immunity. Similar to IL-1α and IL-33, IL-37 is a dual-function cytokine in that IL-37 translocates to the nucleus but also transmits a signal via surface membrane receptors. The role of nuclear IL-37 remains unknown on...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 116; no. 10; pp. 4456 - 4461 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
National Academy of Sciences
05.03.2019
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Abstract | The IL-1 family member IL-37 broadly suppresses innate inflammation and acquired immunity. Similar to IL-1α and IL-33, IL-37 is a dual-function cytokine in that IL-37 translocates to the nucleus but also transmits a signal via surface membrane receptors. The role of nuclear IL-37 remains unknown on the ability of this cytokine to inhibit innate inflammation. Here, we compared suppression of innate inflammation in transgenic mice expressing native human IL-37 (IL-37Tg) with those of transgenic mice carrying the mutation of aspartic acid (D) to alanine (A) at amino acid 20 (IL-37D20ATg). The mutation D20A prevents cleavage of caspase-1, a step required for IL-37 nuclear translocation. In vitro, peritoneal macrophages from IL-37Tg mice reduced LPS-induced IL-1β, IL-6, TNFα and IFNγ by 40–50% whereas in macrophages from IL-37D20ATg mice this suppression was not observed, consistent with loss of nuclear function. Compared with macrophages from IL-37Tg mice, significantly less or no suppression of LPS-induced MAP kinase and NFκB activation was also observed in macrophages from IL-37D20ATg mice. In vivo, levels of IL-1β, IL-6, and TNFα in the lungs and liver were markedly reduced during endotoxemia in IL-37Tg mice but not observed in IL-37D20ATg mice. However, suppression of innate inflammation remains intact in the IL-37D20A mice once the cytokine is released from the cell and binds to its receptor. These studies reveal a nuclear function for suppression of innate inflammation and are consistent with the dual function of IL-37 and a role for caspase-1 in limiting inflammation. |
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AbstractList | The IL-1 family member IL-37 broadly suppresses innate inflammation and acquired immunity. Similar to IL-1α and IL-33, IL-37 is a dual-function cytokine in that IL-37 translocates to the nucleus but also transmits a signal via surface membrane receptors. The role of nuclear IL-37 remains unknown on the ability of this cytokine to inhibit innate inflammation. Here, we compared suppression of innate inflammation in transgenic mice expressing native human IL-37 (IL-37Tg) with those of transgenic mice carrying the mutation of aspartic acid (D) to alanine (A) at amino acid 20 (IL-37D20ATg). The mutation D20A prevents cleavage of caspase-1, a step required for IL-37 nuclear translocation. In vitro, peritoneal macrophages from IL-37Tg mice reduced LPS-induced IL-1β, IL-6, TNFα and IFNγ by 40-50% whereas in macrophages from IL-37D20ATg mice this suppression was not observed, consistent with loss of nuclear function. Compared with macrophages from IL-37Tg mice, significantly less or no suppression of LPS-induced MAP kinase and NFκB activation was also observed in macrophages from IL-37D20ATg mice. In vivo, levels of IL-1β, IL-6, and TNFα in the lungs and liver were markedly reduced during endotoxemia in IL-37Tg mice but not observed in IL-37D20ATg mice. However, suppression of innate inflammation remains intact in the IL-37D20A mice once the cytokine is released from the cell and binds to its receptor. These studies reveal a nuclear function for suppression of innate inflammation and are consistent with the dual function of IL-37 and a role for caspase-1 in limiting inflammation. Significance Interleukin-1 family members are highly inflammatory, but member IL-37 is unique in broadly suppressing inflammation and specific immunity. IL-37 is a dual-function cytokine by binding in the nucleus and to cell surface receptors. We generated an IL-37 transgenic mouse carrying the aspartic acid (D) to alanine (A) mutation at amino acid 20 (D20A), which prevents the nuclear translocation of IL-37. In transgenic mice expressing native IL-37, inflammatory cytokines are reduced during systemic endotoxemia, but, in mice expressing the D20A mutation, protection is lost, consistent with a nuclear function of IL-37. Nevertheless, IL-37D20A released from cells binds to its receptors and initiates suppression of innate inflammation. These studies reveal a nuclear function of IL-37 in vivo. The IL-1 family member IL-37 broadly suppresses innate inflammation and acquired immunity. Similar to IL-1α and IL-33, IL-37 is a dual-function cytokine in that IL-37 translocates to the nucleus but also transmits a signal via surface membrane receptors. The role of nuclear IL-37 remains unknown on the ability of this cytokine to inhibit innate inflammation. Here, we compared suppression of innate inflammation in transgenic mice expressing native human IL-37 (IL-37Tg) with those of transgenic mice carrying the mutation of aspartic acid (D) to alanine (A) at amino acid 20 (IL-37D20ATg). The mutation D20A prevents cleavage of caspase-1, a step required for IL-37 nuclear translocation. In vitro, peritoneal macrophages from IL-37Tg mice reduced LPS-induced IL-1β, IL-6, TNFα and IFNγ by 40–50% whereas in macrophages from IL-37D20ATg mice this suppression was not observed, consistent with loss of nuclear function. Compared with macrophages from IL-37Tg mice, significantly less or no suppression of LPS-induced MAP kinase and NFκB activation was also observed in macrophages from IL-37D20ATg mice. In vivo, levels of IL-1β, IL-6, and TNFα in the lungs and liver were markedly reduced during endotoxemia in IL-37Tg mice but not observed in IL-37D20ATg mice. However, suppression of innate inflammation remains intact in the IL-37D20A mice once the cytokine is released from the cell and binds to its receptor. These studies reveal a nuclear function for suppression of innate inflammation and are consistent with the dual function of IL-37 and a role for caspase-1 in limiting inflammation. Interleukin-1 family members are highly inflammatory, but member IL-37 is unique in broadly suppressing inflammation and specific immunity. IL-37 is a dual-function cytokine by binding in the nucleus and to cell surface receptors. We generated an IL-37 transgenic mouse carrying the aspartic acid (D) to alanine (A) mutation at amino acid 20 (D20A), which prevents the nuclear translocation of IL-37. In transgenic mice expressing native IL-37, inflammatory cytokines are reduced during systemic endotoxemia, but, in mice expressing the D20A mutation, protection is lost, consistent with a nuclear function of IL-37. Nevertheless, IL-37D20A released from cells binds to its receptors and initiates suppression of innate inflammation. These studies reveal a nuclear function of IL-37 in vivo. The IL-1 family member IL-37 broadly suppresses innate inflammation and acquired immunity. Similar to IL-1α and IL-33, IL-37 is a dual-function cytokine in that IL-37 translocates to the nucleus but also transmits a signal via surface membrane receptors. The role of nuclear IL-37 remains unknown on the ability of this cytokine to inhibit innate inflammation. Here, we compared suppression of innate inflammation in transgenic mice expressing native human IL-37 (IL-37Tg) with those of transgenic mice carrying the mutation of aspartic acid (D) to alanine (A) at amino acid 20 (IL-37D20ATg). The mutation D20A prevents cleavage of caspase-1, a step required for IL-37 nuclear translocation. In vitro, peritoneal macrophages from IL-37Tg mice reduced LPS-induced IL-1β, IL-6, TNFα and IFNγ by 40–50% whereas in macrophages from IL-37D20ATg mice this suppression was not observed, consistent with loss of nuclear function. Compared with macrophages from IL-37Tg mice, significantly less or no suppression of LPS-induced MAP kinase and NFκB activation was also observed in macrophages from IL-37D20ATg mice. In vivo, levels of IL-1β, IL-6, and TNFα in the lungs and liver were markedly reduced during endotoxemia in IL-37Tg mice but not observed in IL-37D20ATg mice. However, suppression of innate inflammation remains intact in the IL-37D20A mice once the cytokine is released from the cell and binds to its receptor. These studies reveal a nuclear function for suppression of innate inflammation and are consistent with the dual function of IL-37 and a role for caspase-1 in limiting inflammation. |
Author | Neff, Charles P. López-Vales, Rubén Li, Suzhao Tengesdal, Isak W. Amo-Aparicio, Jesus Azam, Tania Bufler, Philip Palmer, Brent E. Dinarello, Charles A. |
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Keywords | suppression mutation IL-37 inflammation caspase-1 |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Reviewers: D.B., Institute of Protein Biochemistry; and T.C.T., Tufts University School of Medicine. Contributed by Charles A. Dinarello, January 3, 2019 (sent for review December 13, 2018; reviewed by Diana Boraschi and Theoharis C. Theoharides) Author contributions: S.L., J.A.-A., R.L.-V., and C.A.D. designed research; S.L., J.A.-A., C.P.N., I.W.T., T.A., P.B., and C.A.D. performed research; S.L., C.P.N., B.E.P., P.B., and C.A.D. contributed new reagents/analytic tools; S.L., J.A.-A., C.P.N., R.L.-V., and C.A.D. analyzed data; and S.L. and C.A.D. wrote the paper. |
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Snippet | The IL-1 family member IL-37 broadly suppresses innate inflammation and acquired immunity. Similar to IL-1α and IL-33, IL-37 is a dual-function cytokine in... Significance Interleukin-1 family members are highly inflammatory, but member IL-37 is unique in broadly suppressing inflammation and specific immunity. IL-37... Interleukin-1 family members are highly inflammatory, but member IL-37 is unique in broadly suppressing inflammation and specific immunity. IL-37 is a... |
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SubjectTerms | Alanine Amino acids Animals Aspartic acid Biological Sciences Caspase Caspase-1 Cell activation Cell Nucleus - metabolism Cytokines Cytokines - metabolism Endotoxemia Female IL-1β Immunity Immunity, Innate - genetics Inflammation Innate immunity Interleukin 1 Interleukin 6 Interleukin-1 - genetics Interleukin-1 - physiology Lipopolysaccharides Lipopolysaccharides - pharmacology Liver Lungs Macrophages Macrophages, Peritoneal - drug effects Macrophages, Peritoneal - metabolism Male MAP kinase Mice Mice, Inbred C57BL Mice, Transgenic Mutation NF-kappa B - metabolism NF-κB protein Nuclear transport Peritoneum Protein Transport Receptors Rodents Transgenic animals Transgenic mice Translocation Tumor necrosis factor-α γ-Interferon |
Title | Role for nuclear interleukin-37 in the suppression of innate immunity |
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