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Erschienen in: Inflammation 3/2021

07.01.2021 | Review

TRIM Proteins in Inflammation: from Expression to Emerging Regulatory Mechanisms

verfasst von: Luting Yang, Haibin Xia

Erschienen in: Inflammation | Ausgabe 3/2021

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Abstract

Inflammation is an immune response to exogenous or endogenous insults that helps to maintain the tissue homeostasis under stressful conditions. Depending on the differential types of insults, inflammation is classified into microbial, autoimmune, metabolic, allergic, and physical inflammation. With regard to its involvement in the pathogenesis of most of human diseases, dissecting the key molecules in the regulation of inflammatory process is vital for the prevention and therapeutics of human diseases. Tripartite motif (TRIM) proteins are a versatile family of E3 ligases, which are composed of > 80 distinct members in humans recognized for their roles in antiviral responses. Recently, a large number of studies have shown the regulatory roles of TRIM proteins in mediating the inflammation. Herein in this review, we discuss the aberrations of TRIM proteins in autoimmune and autoinflammatory diseases, with a focus on the regulation of different components of inflammatory process, including inflammasome, NF-κB signaling, type I IFN (interferon) production, and Th1/Th17 cell differentiation. Importantly, elucidation of the mechanism underlying the regulation of inflammation by TRIMs provides insights into the use of TRIMs as therapeutic targets for disease treatment.
Literatur
1.
Zurück zum Zitat Hawiger, J., and J. Zienkiewicz. 2019. Decoding inflammation, its causes, genomic responses, and emerging countermeasures. Scandinavian Journal of Immunology 90: e12812–e12812.PubMedPubMedCentral Hawiger, J., and J. Zienkiewicz. 2019. Decoding inflammation, its causes, genomic responses, and emerging countermeasures. Scandinavian Journal of Immunology 90: e12812–e12812.PubMedPubMedCentral
2.
Zurück zum Zitat Zhang, Y., H. Fan, J. Xu, Y. Xiao, Y. Xu, Y. Li, and X. Li. 2013. Network analysis reveals functional cross-links between disease and inflammation genes. Scientific Reports 3: 3426–3426.PubMedPubMedCentral Zhang, Y., H. Fan, J. Xu, Y. Xiao, Y. Xu, Y. Li, and X. Li. 2013. Network analysis reveals functional cross-links between disease and inflammation genes. Scientific Reports 3: 3426–3426.PubMedPubMedCentral
3.
Zurück zum Zitat Rathinam, V.A., and K.A. Fitzgerald. 2016. Inflammasome Complexes: Emerging Mechanisms and Effector Functions. Cell 165: 792–800.PubMedPubMedCentral Rathinam, V.A., and K.A. Fitzgerald. 2016. Inflammasome Complexes: Emerging Mechanisms and Effector Functions. Cell 165: 792–800.PubMedPubMedCentral
4.
Zurück zum Zitat Repa, A., G.K. Bertsias, E. Petraki, C. Choulaki, D. Vassou, K. Kambas, D.T. Boumpas, G. Goulielmos, and P. Sidiropoulos. 2015. Dysregulated production of interleukin-1β upon activation of the NLRP3 inflammasome in patients with familial Mediterranean fever. Human Immunology 76: 488–495.PubMed Repa, A., G.K. Bertsias, E. Petraki, C. Choulaki, D. Vassou, K. Kambas, D.T. Boumpas, G. Goulielmos, and P. Sidiropoulos. 2015. Dysregulated production of interleukin-1β upon activation of the NLRP3 inflammasome in patients with familial Mediterranean fever. Human Immunology 76: 488–495.PubMed
5.
Zurück zum Zitat Gurung, P., and T.-D. Kanneganti. 2016. Autoinflammatory skin disorders: the inflammasome in focus. Trends in Molecular Medicine 22: 545–564.PubMedPubMedCentral Gurung, P., and T.-D. Kanneganti. 2016. Autoinflammatory skin disorders: the inflammasome in focus. Trends in Molecular Medicine 22: 545–564.PubMedPubMedCentral
6.
Zurück zum Zitat Labzin, L.I., M. Bottermann, P. Rodriguez-Silvestre, S. Foss, J.T. Andersen, M. Vaysburd, D. Clift, and L.C. James. 2019. Antibody and DNA sensing pathways converge to activate the inflammasome during primary human macrophage infection. The EMBO Journal 38: e101365.PubMedPubMedCentral Labzin, L.I., M. Bottermann, P. Rodriguez-Silvestre, S. Foss, J.T. Andersen, M. Vaysburd, D. Clift, and L.C. James. 2019. Antibody and DNA sensing pathways converge to activate the inflammasome during primary human macrophage infection. The EMBO Journal 38: e101365.PubMedPubMedCentral
7.
Zurück zum Zitat Coll, R.C. 2019. Role reversal: adaptive immunity instructs inflammasome activation for anti-viral defence. The EMBO Journal 38: e103533.PubMedPubMedCentral Coll, R.C. 2019. Role reversal: adaptive immunity instructs inflammasome activation for anti-viral defence. The EMBO Journal 38: e103533.PubMedPubMedCentral
8.
Zurück zum Zitat Mitoma, H., S. Hanabuchi, T. Kim, M. Bao, Z. Zhang, N. Sugimoto, and Y.J. Liu. 2013. The DHX33 RNA helicase senses cytosolic RNA and activates the NLRP3 inflammasome. Immunity 39: 123–135.PubMedPubMedCentral Mitoma, H., S. Hanabuchi, T. Kim, M. Bao, Z. Zhang, N. Sugimoto, and Y.J. Liu. 2013. The DHX33 RNA helicase senses cytosolic RNA and activates the NLRP3 inflammasome. Immunity 39: 123–135.PubMedPubMedCentral
9.
Zurück zum Zitat Weng, L., H. Mitoma, C. Trichot, M. Bao, Y. Liu, Z. Zhang, and Y.J. Liu. 2014. The E3 ubiquitin ligase tripartite motif 33 is essential for cytosolic RNA-induced NLRP3 inflammasome activation. Journal of Immunology 193: 3676–3682. Weng, L., H. Mitoma, C. Trichot, M. Bao, Y. Liu, Z. Zhang, and Y.J. Liu. 2014. The E3 ubiquitin ligase tripartite motif 33 is essential for cytosolic RNA-induced NLRP3 inflammasome activation. Journal of Immunology 193: 3676–3682.
10.
Zurück zum Zitat Hu, Y., K. Mao, Y. Zeng, S. Chen, Z. Tao, C. Yang, S. Sun, X. Wu, G. Meng, and B. Sun. 2010. Tripartite-motif protein 30 negatively regulates NLRP3 inflammasome activation by modulating reactive oxygen species production. Journal of Immunology 185: 7699–7705. Hu, Y., K. Mao, Y. Zeng, S. Chen, Z. Tao, C. Yang, S. Sun, X. Wu, G. Meng, and B. Sun. 2010. Tripartite-motif protein 30 negatively regulates NLRP3 inflammasome activation by modulating reactive oxygen species production. Journal of Immunology 185: 7699–7705.
11.
Zurück zum Zitat Kimura, T., A. Jain, S.W. Choi, M.A. Mandell, T. Johansen, and V. Deretic. 2017. TRIM-directed selective autophagy regulates immune activation. Autophagy 13: 989–990.PubMed Kimura, T., A. Jain, S.W. Choi, M.A. Mandell, T. Johansen, and V. Deretic. 2017. TRIM-directed selective autophagy regulates immune activation. Autophagy 13: 989–990.PubMed
12.
Zurück zum Zitat Aral, K., E. Berdeli, P.R. Cooper, M.R. Milward, Y. Kapila, B. Karadede Ünal, C.A. Aral, and A. Berdeli. 2020. Differential expression of inflammasome regulatory transcripts in periodontal disease. Journal of Periodontology 91: 606–616.PubMed Aral, K., E. Berdeli, P.R. Cooper, M.R. Milward, Y. Kapila, B. Karadede Ünal, C.A. Aral, and A. Berdeli. 2020. Differential expression of inflammasome regulatory transcripts in periodontal disease. Journal of Periodontology 91: 606–616.PubMed
13.
Zurück zum Zitat Stoler, I., J. Freytag, B. Orak, N. Unterwalder, S. Henning, K. Heim, H. von Bernuth, R. Krüger, S. Winkler, P. Eschenhagen, E. Seipelt, M.A. Mall, D. Foell, C. Kessel, H. Wittkowski, and T. Kallinich. 2020. Gene-dose effect of MEFV gain-of-function mutations determines ex vivo neutrophil activation in familial mediterranean fever. Frontiers in Immunology 11: 716–716.PubMedPubMedCentral Stoler, I., J. Freytag, B. Orak, N. Unterwalder, S. Henning, K. Heim, H. von Bernuth, R. Krüger, S. Winkler, P. Eschenhagen, E. Seipelt, M.A. Mall, D. Foell, C. Kessel, H. Wittkowski, and T. Kallinich. 2020. Gene-dose effect of MEFV gain-of-function mutations determines ex vivo neutrophil activation in familial mediterranean fever. Frontiers in Immunology 11: 716–716.PubMedPubMedCentral
14.
Zurück zum Zitat Kunishita, Y., R. Yoshimi, R. Kamiyama, D. Kishimoto, K. Yoshida, E. Hashimoto, T. Komiya, N. Sakurai, Y. Sugiyama, Y. Kirino, K. Ozato, and H. Nakajima. 2020. TRIM21 dysfunction enhances aberrant B-cell differentiation in autoimmune pathogenesis. Frontiers in Immunology 11: 98–98.PubMedPubMedCentral Kunishita, Y., R. Yoshimi, R. Kamiyama, D. Kishimoto, K. Yoshida, E. Hashimoto, T. Komiya, N. Sakurai, Y. Sugiyama, Y. Kirino, K. Ozato, and H. Nakajima. 2020. TRIM21 dysfunction enhances aberrant B-cell differentiation in autoimmune pathogenesis. Frontiers in Immunology 11: 98–98.PubMedPubMedCentral
15.
Zurück zum Zitat Brauner, S., M. Ivanchenko, G.E. Thorlacius, A. Ambrosi, and M. Wahren-Herlenius. 2018. The Sjögren's syndrome-associated autoantigen Ro52/TRIM21 modulates follicular B cell homeostasis and immunoglobulin production. Clinical and Experimental Immunology 194: 315–326.PubMedPubMedCentral Brauner, S., M. Ivanchenko, G.E. Thorlacius, A. Ambrosi, and M. Wahren-Herlenius. 2018. The Sjögren's syndrome-associated autoantigen Ro52/TRIM21 modulates follicular B cell homeostasis and immunoglobulin production. Clinical and Experimental Immunology 194: 315–326.PubMedPubMedCentral
16.
17.
Zurück zum Zitat Niida, M., M. Tanaka, and T. Kamitani. 2010. Downregulation of active IKK beta by Ro52-mediated autophagy. Molecular Immunology 47: 2378–2387.PubMedPubMedCentral Niida, M., M. Tanaka, and T. Kamitani. 2010. Downregulation of active IKK beta by Ro52-mediated autophagy. Molecular Immunology 47: 2378–2387.PubMedPubMedCentral
18.
Zurück zum Zitat Shi, M., H. Cho, K.-S. Inn, A. Yang, Z. Zhao, Q. Liang, G.A. Versteeg, S. Amini-Bavil-Olyaee, L.-Y. Wong, B.V. Zlokovic, H.S. Park, A. García-Sastre, and J.U. Jung. 2014. Negative regulation of NF-κB activity by brain-specific TRIpartite Motif protein 9. Nature Communications 5: 4820–4820.PubMedPubMedCentral Shi, M., H. Cho, K.-S. Inn, A. Yang, Z. Zhao, Q. Liang, G.A. Versteeg, S. Amini-Bavil-Olyaee, L.-Y. Wong, B.V. Zlokovic, H.S. Park, A. García-Sastre, and J.U. Jung. 2014. Negative regulation of NF-κB activity by brain-specific TRIpartite Motif protein 9. Nature Communications 5: 4820–4820.PubMedPubMedCentral
19.
Zurück zum Zitat Sun, M., S. Li, K. Yu, J. Xiang, and F. Li. 2019. An E3 ubiquitin ligase TRIM9 is involved in WSSV infection via interaction with beta-TrCP. Developmental and Comparative Immunology 97: 57–63.PubMed Sun, M., S. Li, K. Yu, J. Xiang, and F. Li. 2019. An E3 ubiquitin ligase TRIM9 is involved in WSSV infection via interaction with beta-TrCP. Developmental and Comparative Immunology 97: 57–63.PubMed
20.
Zurück zum Zitat Jang, H.-D., H.Z. Hwang, H.-S. Kim, and S.Y. Lee. 2019. C-Cbl negatively regulates TRAF6-mediated NF-κB activation by promoting K48-linked polyubiquitination of TRAF6. Cellular & Molecular Biology Letters 24: 29–29. Jang, H.-D., H.Z. Hwang, H.-S. Kim, and S.Y. Lee. 2019. C-Cbl negatively regulates TRAF6-mediated NF-κB activation by promoting K48-linked polyubiquitination of TRAF6. Cellular & Molecular Biology Letters 24: 29–29.
21.
Zurück zum Zitat Chang, T.-H., R. Yoshimi, and K. Ozato. 2015. Tripartite motif (TRIM) 12c, a mouse homolog of TRIM5, is a ubiquitin ligase that stimulates type I IFN and NF-κB pathways along with TNFR-associated factor 6. Journal of Immunology (Baltimore, Md. : 1950) 195: 5367–5379. Chang, T.-H., R. Yoshimi, and K. Ozato. 2015. Tripartite motif (TRIM) 12c, a mouse homolog of TRIM5, is a ubiquitin ligase that stimulates type I IFN and NF-κB pathways along with TNFR-associated factor 6. Journal of Immunology (Baltimore, Md. : 1950) 195: 5367–5379.
22.
Zurück zum Zitat Zhao, W., L. Wang, M. Zhang, C. Yuan, and C. Gao. 2012. E3 ubiquitin ligase tripartite motif 38 negatively regulates TLR-mediated immune responses by proteasomal degradation of TNF receptor-associated factor 6 in macrophages. Journal of Immunology 188: 2567–2574. Zhao, W., L. Wang, M. Zhang, C. Yuan, and C. Gao. 2012. E3 ubiquitin ligase tripartite motif 38 negatively regulates TLR-mediated immune responses by proteasomal degradation of TNF receptor-associated factor 6 in macrophages. Journal of Immunology 188: 2567–2574.
23.
Zurück zum Zitat Huang, X., Y. Li, X. Li, D. Fan, H.B. Xin, and M. Fu. 2020. TRIM14 promotes endothelial activation via activating NF-kappaB signaling pathway. Journal of Molecular Cell Biology 12: 176–189.PubMed Huang, X., Y. Li, X. Li, D. Fan, H.B. Xin, and M. Fu. 2020. TRIM14 promotes endothelial activation via activating NF-kappaB signaling pathway. Journal of Molecular Cell Biology 12: 176–189.PubMed
24.
Zurück zum Zitat Noguchi, K., F. Okumura, N. Takahashi, A. Kataoka, T. Kamiyama, S. Todo, and S. Hatakeyama. 2011. TRIM40 promotes neddylation of IKKgamma and is downregulated in gastrointestinal cancers. Carcinogenesis 32: 995–1004.PubMed Noguchi, K., F. Okumura, N. Takahashi, A. Kataoka, T. Kamiyama, S. Todo, and S. Hatakeyama. 2011. TRIM40 promotes neddylation of IKKgamma and is downregulated in gastrointestinal cancers. Carcinogenesis 32: 995–1004.PubMed
25.
Zurück zum Zitat Qiu, H., F. Huang, H. Xiao, B. Sun, and R. Yang. 2013. TRIM22 inhibits the TRAF6-stimulated NF-kappaB pathway by targeting TAB2 for degradation. Virologica Sinica 28: 209–215.PubMed Qiu, H., F. Huang, H. Xiao, B. Sun, and R. Yang. 2013. TRIM22 inhibits the TRAF6-stimulated NF-kappaB pathway by targeting TAB2 for degradation. Virologica Sinica 28: 209–215.PubMed
26.
Zurück zum Zitat Shi, M., W. Deng, E. Bi, K. Mao, Y. Ji, G. Lin, X. Wu, Z. Tao, Z. Li, X. Cai, S. Sun, C. Xiang, and B. Sun. 2008. TRIM30α negatively regulates TLR-mediated NF-κB activation by targeting TAB2 and TAB3 for degradation. Nature Immunology 9: 369–377.PubMed Shi, M., W. Deng, E. Bi, K. Mao, Y. Ji, G. Lin, X. Wu, Z. Tao, Z. Li, X. Cai, S. Sun, C. Xiang, and B. Sun. 2008. TRIM30α negatively regulates TLR-mediated NF-κB activation by targeting TAB2 and TAB3 for degradation. Nature Immunology 9: 369–377.PubMed
27.
Zurück zum Zitat Matsuda, A., Y. Suzuki, G. Honda, S. Muramatsu, O. Matsuzaki, Y. Nagano, T. Doi, K. Shimotohno, T. Harada, E. Nishida, H. Hayashi, and S. Sugano. 2003. Large-scale identification and characterization of human genes that activate NF-κB and MAPK signaling pathways. Oncogene 22: 3307–3318.PubMed Matsuda, A., Y. Suzuki, G. Honda, S. Muramatsu, O. Matsuzaki, Y. Nagano, T. Doi, K. Shimotohno, T. Harada, E. Nishida, H. Hayashi, and S. Sugano. 2003. Large-scale identification and characterization of human genes that activate NF-κB and MAPK signaling pathways. Oncogene 22: 3307–3318.PubMed
28.
Zurück zum Zitat Kim, K., J.H. Kim, I. Kim, S. Seong, and N. Kim. 2018. TRIM38 regulates NF-kappaB activation through TAB2 degradation in osteoclast and osteoblast differentiation. Bone 113: 17–28.PubMed Kim, K., J.H. Kim, I. Kim, S. Seong, and N. Kim. 2018. TRIM38 regulates NF-kappaB activation through TAB2 degradation in osteoclast and osteoblast differentiation. Bone 113: 17–28.PubMed
29.
Zurück zum Zitat Hu, M.-M., Q. Yang, J. Zhang, S.-M. Liu, Y. Zhang, H. Lin, Z.-F. Huang, Y.-Y. Wang, X.-D. Zhang, B. Zhong, and H.-B. Shu. 2014. TRIM38 inhibits TNFα- and IL-1β–triggered NF-κB activation by mediating lysosome-dependent degradation of TAB2/3. Proceedings of the National Academy of Sciences 111: 1509–1514. Hu, M.-M., Q. Yang, J. Zhang, S.-M. Liu, Y. Zhang, H. Lin, Z.-F. Huang, Y.-Y. Wang, X.-D. Zhang, B. Zhong, and H.-B. Shu. 2014. TRIM38 inhibits TNFα- and IL-1β–triggered NF-κB activation by mediating lysosome-dependent degradation of TAB2/3. Proceedings of the National Academy of Sciences 111: 1509–1514.
30.
Zurück zum Zitat Shibata, M., T. Sato, R. Nukiwa, T. Ariga, and S. Hatakeyama. 2012. TRIM45 negatively regulates NF-kappaB-mediated transcription and suppresses cell proliferation. Biochemical and Biophysical Research Communications 423: 104–109.PubMed Shibata, M., T. Sato, R. Nukiwa, T. Ariga, and S. Hatakeyama. 2012. TRIM45 negatively regulates NF-kappaB-mediated transcription and suppresses cell proliferation. Biochemical and Biophysical Research Communications 423: 104–109.PubMed
31.
Zurück zum Zitat Hao, M.Q., L.J. Xie, W. Leng, and R.W. Xue. 2019. Trim47 is a critical regulator of cerebral ischemia-reperfusion injury through regulating apoptosis and inflammation. Biochemical and Biophysical Research Communications 515: 651–657.PubMed Hao, M.Q., L.J. Xie, W. Leng, and R.W. Xue. 2019. Trim47 is a critical regulator of cerebral ischemia-reperfusion injury through regulating apoptosis and inflammation. Biochemical and Biophysical Research Communications 515: 651–657.PubMed
32.
Zurück zum Zitat Bai, X., Y.-L. Zhang, and L.-N. Liu. 2020. Inhibition of TRIM8 restrains ischaemia-reperfusion-mediated cerebral injury by regulation of NF-κB activation associated inflammation and apoptosis. Experimental Cell Research 388: 111818.PubMed Bai, X., Y.-L. Zhang, and L.-N. Liu. 2020. Inhibition of TRIM8 restrains ischaemia-reperfusion-mediated cerebral injury by regulation of NF-κB activation associated inflammation and apoptosis. Experimental Cell Research 388: 111818.PubMed
33.
Zurück zum Zitat Muskardin, T.L.W., and T.B. Niewold. 2018. Type I interferon in rheumatic diseases. Nature Reviews Rheumatology 14: 214–228.PubMedPubMedCentral Muskardin, T.L.W., and T.B. Niewold. 2018. Type I interferon in rheumatic diseases. Nature Reviews Rheumatology 14: 214–228.PubMedPubMedCentral
34.
Zurück zum Zitat Higgs, R., J. Ní Gabhann, N. Ben Larbi, E.P. Breen, K.A. Fitzgerald, and C.A. Jefferies. 2008. The E3 ubiquitin ligase Ro52 negatively regulates IFN-beta production post-pathogen recognition by polyubiquitin-mediated degradation of IRF3. Journal of Immunology (Baltimore, Md. : 1950) 181: 1780–1786. Higgs, R., J. Ní Gabhann, N. Ben Larbi, E.P. Breen, K.A. Fitzgerald, and C.A. Jefferies. 2008. The E3 ubiquitin ligase Ro52 negatively regulates IFN-beta production post-pathogen recognition by polyubiquitin-mediated degradation of IRF3. Journal of Immunology (Baltimore, Md. : 1950) 181: 1780–1786.
35.
Zurück zum Zitat Tan, T., and L. Xia. 2020. TRIM21 Aggravates herpes simplex virus epithelial keratitis by attenuating STING-IRF3-mediated type I interferon signaling. Frontiers in Microbiology 11: 703–703.PubMedPubMedCentral Tan, T., and L. Xia. 2020. TRIM21 Aggravates herpes simplex virus epithelial keratitis by attenuating STING-IRF3-mediated type I interferon signaling. Frontiers in Microbiology 11: 703–703.PubMedPubMedCentral
36.
Zurück zum Zitat Stacey, K.B., E. Breen, and C.A. Jefferies. 2012. Tyrosine phosphorylation of the E3 ubiquitin ligase TRIM21 positively regulates interaction with IRF3 and hence TRIM21 activity. PLoS One 7: e34041.PubMedPubMedCentral Stacey, K.B., E. Breen, and C.A. Jefferies. 2012. Tyrosine phosphorylation of the E3 ubiquitin ligase TRIM21 positively regulates interaction with IRF3 and hence TRIM21 activity. PLoS One 7: e34041.PubMedPubMedCentral
37.
Zurück zum Zitat Maarifi, G., N. Smith, S. Maillet, O. Moncorgé, C. Chamontin, J. Edouard, F. Sohm, F.P. Blanchet, J.-P. Herbeuval, G. Lutfalla, et al. 2019. TRIM8 is required for virus-induced IFN response in human plasmacytoid dendritic cells. Science Advances 5: eaax3511.PubMedPubMedCentral Maarifi, G., N. Smith, S. Maillet, O. Moncorgé, C. Chamontin, J. Edouard, F. Sohm, F.P. Blanchet, J.-P. Herbeuval, G. Lutfalla, et al. 2019. TRIM8 is required for virus-induced IFN response in human plasmacytoid dendritic cells. Science Advances 5: eaax3511.PubMedPubMedCentral
38.
Zurück zum Zitat Wu, M., C. Dan, J.F. Gui, and Y.B. Zhang. 2019. Fish species-specific TRIM gene FTRCA1 negatively regulates interferon response through attenuating IRF7 transcription. Fish & Shellfish Immunology 90: 180–187. Wu, M., C. Dan, J.F. Gui, and Y.B. Zhang. 2019. Fish species-specific TRIM gene FTRCA1 negatively regulates interferon response through attenuating IRF7 transcription. Fish & Shellfish Immunology 90: 180–187.
39.
Zurück zum Zitat Kondo, T., M. Watanabe, and S. Hatakeyama. 2012. TRIM59 interacts with ECSIT and negatively regulates NF-kappaB and IRF-3/7-mediated signal pathways. Biochemical and Biophysical Research Communications 422: 501–507.PubMed Kondo, T., M. Watanabe, and S. Hatakeyama. 2012. TRIM59 interacts with ECSIT and negatively regulates NF-kappaB and IRF-3/7-mediated signal pathways. Biochemical and Biophysical Research Communications 422: 501–507.PubMed
40.
Zurück zum Zitat Zhao, W., L. Wang, M. Zhang, P. Wang, C. Yuan, J. Qi, H. Meng, and C. Gao. 2012. Tripartite motif-containing protein 38 negatively regulates TLR3/4- and RIG-I-mediated IFN-beta production and antiviral response by targeting NAP1. Journal of Immunology 188: 5311–5318. Zhao, W., L. Wang, M. Zhang, P. Wang, C. Yuan, J. Qi, H. Meng, and C. Gao. 2012. Tripartite motif-containing protein 38 negatively regulates TLR3/4- and RIG-I-mediated IFN-beta production and antiviral response by targeting NAP1. Journal of Immunology 188: 5311–5318.
41.
Zurück zum Zitat Hu, M.M., X.Q. Xie, Q. Yang, C.Y. Liao, W. Ye, H. Lin, and H.B. Shu. 2015. TRIM38 negatively regulates TLR3/4-mediated innate immune and inflammatory responses by two sequential and distinct mechanisms. Journal of Immunology 195: 4415–4425. Hu, M.M., X.Q. Xie, Q. Yang, C.Y. Liao, W. Ye, H. Lin, and H.B. Shu. 2015. TRIM38 negatively regulates TLR3/4-mediated innate immune and inflammatory responses by two sequential and distinct mechanisms. Journal of Immunology 195: 4415–4425.
42.
Zurück zum Zitat Xue, Q., Z. Zhou, X. Lei, X. Liu, B. He, J. Wang, and T. Hung. 2012. TRIM38 negatively regulates TLR3-mediated IFN-beta signaling by targeting TRIF for degradation. PLoS One 7: e46825.PubMedPubMedCentral Xue, Q., Z. Zhou, X. Lei, X. Liu, B. He, J. Wang, and T. Hung. 2012. TRIM38 negatively regulates TLR3-mediated IFN-beta signaling by targeting TRIF for degradation. PLoS One 7: e46825.PubMedPubMedCentral
43.
Zurück zum Zitat Bhaumik, S., and R. Basu. 2017. Cellular and molecular dynamics of Th17 differentiation and its developmental plasticity in the intestinal immune response. Frontiers in Immunology 8: 254–254.PubMedPubMedCentral Bhaumik, S., and R. Basu. 2017. Cellular and molecular dynamics of Th17 differentiation and its developmental plasticity in the intestinal immune response. Frontiers in Immunology 8: 254–254.PubMedPubMedCentral
44.
Zurück zum Zitat Kotschenreuther, K., I. Waqué, S. Yan, A. Meyer, T. Haak, J. von Tresckow, J. Schiller, L. Gloyer, M. Dittrich-Salamon, and D.M. Kofler. 2020. Cannabinoids drive Th17 cell differentiation in patients with rheumatic autoimmune diseases. Cellular & Molecular Immunology. https://doi.org/10.1038/s41423-020-0437-4.CrossRef Kotschenreuther, K., I. Waqué, S. Yan, A. Meyer, T. Haak, J. von Tresckow, J. Schiller, L. Gloyer, M. Dittrich-Salamon, and D.M. Kofler. 2020. Cannabinoids drive Th17 cell differentiation in patients with rheumatic autoimmune diseases. Cellular & Molecular Immunology. https://​doi.​org/​10.​1038/​s41423-020-0437-4.CrossRef
45.
Zurück zum Zitat Espinosa, A., V. Dardalhon, S. Brauner, A. Ambrosi, R. Higgs, F.J. Quintana, M. Sjöstrand, M.-L. Eloranta, J. Ní Gabhann, O. Winqvist, B. Sundelin, C.A. Jefferies, B. Rozell, V.K. Kuchroo, and M. Wahren-Herlenius. 2009. Loss of the lupus autoantigen Ro52/Trim21 induces tissue inflammation and systemic autoimmunity by disregulating the IL-23-Th17 pathway. The Journal of Experimental Medicine 206: 1661–1671.PubMedPubMedCentral Espinosa, A., V. Dardalhon, S. Brauner, A. Ambrosi, R. Higgs, F.J. Quintana, M. Sjöstrand, M.-L. Eloranta, J. Ní Gabhann, O. Winqvist, B. Sundelin, C.A. Jefferies, B. Rozell, V.K. Kuchroo, and M. Wahren-Herlenius. 2009. Loss of the lupus autoantigen Ro52/Trim21 induces tissue inflammation and systemic autoimmunity by disregulating the IL-23-Th17 pathway. The Journal of Experimental Medicine 206: 1661–1671.PubMedPubMedCentral
46.
Zurück zum Zitat Brauner, S., X. Jiang, G.E. Thorlacius, A.M. Lundberg, T. Östberg, Z.-Q. Yan, V.K. Kuchroo, G.K. Hansson, and M. Wahren-Herlenius. 2017. Augmented Th17 differentiation in Trim21 deficiency promotes a stable phenotype of atherosclerotic plaques with high collagen content. Cardiovascular Research 114: 158–167. Brauner, S., X. Jiang, G.E. Thorlacius, A.M. Lundberg, T. Östberg, Z.-Q. Yan, V.K. Kuchroo, G.K. Hansson, and M. Wahren-Herlenius. 2017. Augmented Th17 differentiation in Trim21 deficiency promotes a stable phenotype of atherosclerotic plaques with high collagen content. Cardiovascular Research 114: 158–167.
47.
Zurück zum Zitat Zhou, G., W. Wu, L. Yu, T. Yu, W. Yang, P. Wang, X. Zhang, Y. Cong, and Z. Liu. 2018. Tripartite motif-containing (TRIM) 21 negatively regulates intestinal mucosal inflammation through inhibiting TH1/TH17 cell differentiation in patients with inflammatory bowel diseases. Journal of Allergy and Clinical Immunology 142: 1218–1228.e1212. Zhou, G., W. Wu, L. Yu, T. Yu, W. Yang, P. Wang, X. Zhang, Y. Cong, and Z. Liu. 2018. Tripartite motif-containing (TRIM) 21 negatively regulates intestinal mucosal inflammation through inhibiting TH1/TH17 cell differentiation in patients with inflammatory bowel diseases. Journal of Allergy and Clinical Immunology 142: 1218–1228.e1212.
48.
Zurück zum Zitat Ahn, Y., J.-H. Hwang, Z. Zheng, D. Bang, and D.-Y. Kim. 2017. Enhancement of Th1/Th17 inflammation by TRIM21 in Behçet's disease. Scientific Reports 7: 3018–3018.PubMedPubMedCentral Ahn, Y., J.-H. Hwang, Z. Zheng, D. Bang, and D.-Y. Kim. 2017. Enhancement of Th1/Th17 inflammation by TRIM21 in Behçet's disease. Scientific Reports 7: 3018–3018.PubMedPubMedCentral
49.
Zurück zum Zitat Perez-Lloret, J., I.S. Okoye, R. Guidi, Y. Kannan, S.M. Coomes, S. Czieso, G. Mengus, I. Davidson, and M.S. Wilson. 2016. T-cell-intrinsic Tif1α/Trim24 regulates IL-1R expression on TH2 cells and TH2 cell-mediated airway allergy. Proceedings of the National Academy of Sciences of the United States of America 113: E568–E576.PubMedPubMedCentral Perez-Lloret, J., I.S. Okoye, R. Guidi, Y. Kannan, S.M. Coomes, S. Czieso, G. Mengus, I. Davidson, and M.S. Wilson. 2016. T-cell-intrinsic Tif1α/Trim24 regulates IL-1R expression on TH2 cells and TH2 cell-mediated airway allergy. Proceedings of the National Academy of Sciences of the United States of America 113: E568–E576.PubMedPubMedCentral
50.
Zurück zum Zitat Yang, L., L. Jin, Y. Ke, X. Fan, T. Zhang, C. Zhang, H. Bian, and G. Wang. 2018. E3 Ligase Trim21 ubiquitylates and stabilizes keratin 17 to induce STAT3 activation in psoriasis. The Journal of Investigative Dermatology 138: 2568–2577.PubMed Yang, L., L. Jin, Y. Ke, X. Fan, T. Zhang, C. Zhang, H. Bian, and G. Wang. 2018. E3 Ligase Trim21 ubiquitylates and stabilizes keratin 17 to induce STAT3 activation in psoriasis. The Journal of Investigative Dermatology 138: 2568–2577.PubMed
51.
Zurück zum Zitat Vinter, H., A. Langkilde, V. Ottosson, A. Espinosa, M. Wahren-Herlenius, L. Raaby, C. Johansen, and L. Iversen. 2017. TRIM21 is important in the early phase of inflammation in the imiquimod-induced psoriasis-like skin inflammation mouse model. Experimental Dermatology 26: 713–720.PubMed Vinter, H., A. Langkilde, V. Ottosson, A. Espinosa, M. Wahren-Herlenius, L. Raaby, C. Johansen, and L. Iversen. 2017. TRIM21 is important in the early phase of inflammation in the imiquimod-induced psoriasis-like skin inflammation mouse model. Experimental Dermatology 26: 713–720.PubMed
52.
Zurück zum Zitat Liu, Y., J.P. Lagowski, S. Gao, J.H. Raymond, C.R. White, and M.F. Kulesz-Martin. 2010. Regulation of the psoriatic chemokine CCL20 by E3 ligases Trim32 and Piasy in keratinocytes. The Journal of Investigative Dermatology 130: 1384–1390.PubMedPubMedCentral Liu, Y., J.P. Lagowski, S. Gao, J.H. Raymond, C.R. White, and M.F. Kulesz-Martin. 2010. Regulation of the psoriatic chemokine CCL20 by E3 ligases Trim32 and Piasy in keratinocytes. The Journal of Investigative Dermatology 130: 1384–1390.PubMedPubMedCentral
53.
Zurück zum Zitat Liu, Y., Z. Wang, R. De La Torre, A. Barling, T. Tsujikawa, N. Hornick, J. Hanifin, E. Simpson, Y. Wang, E. Swanzey, et al. 2017. Trim32 deficiency enhances Th2 immunity and predisposes to features of atopic dermatitis. The Journal of Investigative Dermatology 137: 359–366.PubMed Liu, Y., Z. Wang, R. De La Torre, A. Barling, T. Tsujikawa, N. Hornick, J. Hanifin, E. Simpson, Y. Wang, E. Swanzey, et al. 2017. Trim32 deficiency enhances Th2 immunity and predisposes to features of atopic dermatitis. The Journal of Investigative Dermatology 137: 359–366.PubMed
54.
Zurück zum Zitat Espinosa, A., W. Zhou, M. Ek, M. Hedlund, S. Brauner, K. Popovic, L. Horvath, T. Wallerskog, M. Oukka, F. Nyberg, V.K. Kuchroo, and M. Wahren-Herlenius. 2006. The Sjogren's syndrome-associated autoantigen Ro52 is an E3 ligase that regulates proliferation and cell death. Journal of Immunology 176: 6277–6285. Espinosa, A., W. Zhou, M. Ek, M. Hedlund, S. Brauner, K. Popovic, L. Horvath, T. Wallerskog, M. Oukka, F. Nyberg, V.K. Kuchroo, and M. Wahren-Herlenius. 2006. The Sjogren's syndrome-associated autoantigen Ro52 is an E3 ligase that regulates proliferation and cell death. Journal of Immunology 176: 6277–6285.
55.
Zurück zum Zitat Smith, S., J. Ni Gabhann, E. McCarthy, B. Coffey, R. Mahony, J.C. Byrne, K. Stacey, E. Ball, A. Bell, G. Cunnane, et al. 2014. Estrogen receptor alpha regulates tripartite motif-containing protein 21 expression, contributing to dysregulated cytokine production in systemic lupus erythematosus. Arthritis & Rhematology 66: 163–172. Smith, S., J. Ni Gabhann, E. McCarthy, B. Coffey, R. Mahony, J.C. Byrne, K. Stacey, E. Ball, A. Bell, G. Cunnane, et al. 2014. Estrogen receptor alpha regulates tripartite motif-containing protein 21 expression, contributing to dysregulated cytokine production in systemic lupus erythematosus. Arthritis & Rhematology 66: 163–172.
56.
Zurück zum Zitat Kurata, R., H. Nakaoka, A. Tajima, K. Hosomichi, T. Shiina, A. Meguro, N. Mizuki, S. Ohono, I. Inoue, and H. Inoko. 2010. TRIM39 and RNF39 are associated with Behcet's disease independently of HLA-B *51 and -A *26. Biochemical and Biophysical Research Communications 401: 533–537.PubMed Kurata, R., H. Nakaoka, A. Tajima, K. Hosomichi, T. Shiina, A. Meguro, N. Mizuki, S. Ohono, I. Inoue, and H. Inoko. 2010. TRIM39 and RNF39 are associated with Behcet's disease independently of HLA-B *51 and -A *26. Biochemical and Biophysical Research Communications 401: 533–537.PubMed
57.
Zurück zum Zitat Hu, M.-M., and H.-B. Shu. 2017. Multifaceted roles of TRIM38 in innate immune and inflammatory responses. Cellular & Molecular Immunology 14: 331–338. Hu, M.-M., and H.-B. Shu. 2017. Multifaceted roles of TRIM38 in innate immune and inflammatory responses. Cellular & Molecular Immunology 14: 331–338.
Metadaten
Titel
TRIM Proteins in Inflammation: from Expression to Emerging Regulatory Mechanisms
verfasst von
Luting Yang
Haibin Xia
Publikationsdatum
07.01.2021
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 3/2021
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-020-01394-8

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