{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T15:27:50Z","timestamp":1772119670312,"version":"3.50.1"},"reference-count":47,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T00:00:00Z","timestamp":1768867200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,2,9]],"date-time":"2026-02-09T00:00:00Z","timestamp":1770595200000},"content-version":"vor","delay-in-days":20,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81801988"],"award-info":[{"award-number":["81801988"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81801884"],"award-info":[{"award-number":["81801884"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"The Innovation Cultivation Fund of the Sixth Medical Center of Chinese PLA General Hospital","award":["CXPY202001"],"award-info":[{"award-number":["CXPY202001"]}]},{"name":"The Independent Innovation Science Fund Project of the Fourth Medical Center of Chinese PLA General Hospital","award":["2024-4ZX-ZD-10"],"award-info":[{"award-number":["2024-4ZX-ZD-10"]}]}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Inflammation"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Despite the well-recognized role of the deubiquitinase CYLD in the pathogenesis of tumors and certain inflammatory diseases, its specific function and regulatory mechanisms in psoriasis remain unclear. Thus, we first analyzed CYLD expression differences between psoriatic patients and healthy controls using skin samples from the GEO database and validated its expression dynamics in an imiquimod (IMQ)-induced mouse model. Then, we systematically evaluated the effects of CYLD deficiency on psoriasiform inflammation through histopathology, immunohistochemistry, RNA sequencing, and immunofluorescence analyses using Cyld knockout (\n                    <jats:italic>Cyld<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    ) mice, and employed bioinformatics approaches including CIBERSORT and Weighted Gene Co-expression Network Analysis (WGCNA) to further explore the associations between CYLD and neutrophil-related pathways and genes. The results showed that CYLD expression was significantly upregulated in lesional skin of psoriasis patients;\n                    <jats:italic>Cyld<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice displayed more severe psoriasiform symptoms (enhanced epidermal thickening, increased neutrophil infiltration, significantly augmented formation of neutrophil extracellular traps [NETs]); CYLD deficiency led to excessive activation of the NF-\u03baB signaling pathway and upregulated expression of various pro-inflammatory cytokines and chemokines. Bioinformatics analyses confirmed CYLD was closely associated with pathways related to neutrophil migration and activation. These findings lead to the conclusion that CYLD plays a crucial negative regulatory role in psoriasis by inhibiting NF-\u03baB-mediated neutrophil activation and NETs formation, so targeted activation of CYLD may represent a promising novel therapeutic strategy for psoriasis.\n                  <\/jats:p>","DOI":"10.1007\/s10753-026-02452-3","type":"journal-article","created":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T18:35:31Z","timestamp":1768934131000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["CYLD Limits Neutrophil-Driven Psoriatic Inflammation"],"prefix":"10.1007","volume":"49","author":[{"given":"Zhenzong","family":"Fa","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zeping","family":"Huang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yi","family":"Shang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yang","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qun","family":"Xie","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Runping","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2026,1,20]]},"reference":[{"issue":"3","key":"2452_CR1","doi-asserted-by":"publisher","first-page":"377","DOI":"10.1016\/j.jaad.2016.07.064","volume":"76","author":"J Takeshita","year":"2017","unstructured":"Takeshita, J., S. Grewal, S. M. Langan, N. N. Mehta, A. Ogdie, and A. S. Van Voorhees et al. 2017. Psoriasis and comorbid diseases: Epidemiology. Journal of the American Academy of Dermatology 76(3):377\u2013390. https:\/\/doi.org\/10.1016\/j.jaad.2016.07.064","journal-title":"Journal of the American Academy of Dermatology"},{"key":"2452_CR2","doi-asserted-by":"publisher","first-page":"1643418","DOI":"10.3389\/fimmu.2025.1643418","volume":"16","author":"Y Yao","year":"2025","unstructured":"Yao, Y., L-Q. Chen, Y-B. Lv, S-L. Tang, W. Shen, and H. Sun et al. 2025. Skin immune microenvironment in psoriasis: From bench to bedside. Frontiers in Immunology 16:1643418. https:\/\/doi.org\/10.3389\/fimmu.2025.1643418","journal-title":"Frontiers in Immunology"},{"issue":"1","key":"2452_CR3","doi-asserted-by":"publisher","first-page":"45","DOI":"10.1038\/s41572-025-00630-5","volume":"11","author":"AW Armstrong","year":"2025","unstructured":"Armstrong, A. W., A. Blauvelt, K. Callis Duffin, Y-H. Huang, L. J. Savage, and L. Guo et al. 2025. Psoriasis. Nature Reviews Disease Primers 11(1):45. https:\/\/doi.org\/10.1038\/s41572-025-00630-5","journal-title":"Nature Reviews Disease Primers"},{"key":"2452_CR4","doi-asserted-by":"publisher","first-page":"1047367","DOI":"10.3389\/fimmu.2022.1047367","volume":"13","author":"J Wu","year":"2022","unstructured":"Wu, J., F. Zhang, X. Zheng, J. Zhang, P. Cao, and Z. Sun et al. 2022. Identification of renal ischemia reperfusion injury subtypes and predictive strategies for delayed graft function and graft survival based on neutrophil extracellular trap-related genes. Frontiers in Immunology 13:1047367. https:\/\/doi.org\/10.3389\/fimmu.2022.1047367","journal-title":"Frontiers in Immunology"},{"key":"2452_CR5","doi-asserted-by":"publisher","first-page":"110308","DOI":"10.1016\/j.clim.2024.110308","volume":"266","author":"R Li","year":"2024","unstructured":"Li, R., Y. Xiong, L. Ma, C. Peng, S. Qi, and R. Gao et al. 2024. Neutrophil extracellular traps promote macrophage inflammation in psoriasis. Clinical Immunology (Orlando Fla 266:110308. https:\/\/doi.org\/10.1016\/j.clim.2024.110308","journal-title":"Clinical Immunology (Orlando Fla"},{"key":"2452_CR6","doi-asserted-by":"publisher","first-page":"3709749","DOI":"10.1155\/2020\/3709749","volume":"2020","author":"W-M Wang","year":"2020","unstructured":"Wang, W-M., and H-Z. Jin. 2020. Role of neutrophils in psoriasis. Journal of Immunology Research 2020:3709749. https:\/\/doi.org\/10.1155\/2020\/3709749","journal-title":"Journal of Immunology Research"},{"key":"2452_CR7","doi-asserted-by":"publisher","first-page":"2376","DOI":"10.3389\/fimmu.2019.02376","volume":"10","author":"C-C Chiang","year":"2019","unstructured":"Chiang, C-C., W-J. Cheng, M. Korinek, C-Y. Lin, and T-L. Hwang. 2019. Neutrophils in psoriasis. Frontiers in Immunology 10:2376. https:\/\/doi.org\/10.3389\/fimmu.2019.02376","journal-title":"Frontiers in Immunology"},{"key":"2452_CR8","doi-asserted-by":"publisher","first-page":"746","DOI":"10.3389\/fimmu.2019.00746","volume":"10","author":"S Shao","year":"2019","unstructured":"Shao, S., H. Fang, E. Dang, K. Xue, J. Zhang, and B. Li et al. 2019. Neutrophil extracellular traps promote inflammatory responses in psoriasis via activating epidermal TLR4\/IL-36R crosstalk. Frontiers in Immunology 10:746. https:\/\/doi.org\/10.3389\/fimmu.2019.00746","journal-title":"Frontiers in Immunology"},{"issue":"1","key":"2452_CR9","doi-asserted-by":"publisher","first-page":"105","DOI":"10.1038\/s41467-019-13756-4","volume":"11","author":"F Herster","year":"2020","unstructured":"Herster, F., Z. Bittner, N. K. Archer, S. Dickh\u00f6fer, D. Eisel, and T. Eigenbrod et al. 2020. Neutrophil extracellular trap-associated RNA and LL37 enable self-amplifying inflammation in psoriasis. Nature Communications 11(1):105. https:\/\/doi.org\/10.1038\/s41467-019-13756-4","journal-title":"Nature Communications"},{"issue":"1","key":"2452_CR10","doi-asserted-by":"publisher","first-page":"490","DOI":"10.4049\/jimmunol.1100123","volume":"187","author":"AM Lin","year":"2011","unstructured":"Lin, A. M., C. J. Rubin, R. Khandpur, J. Y. Wang, M. Riblett, and S. Yalavarthi et al. 2011. Mast cells and neutrophils release IL-17 through extracellular trap formation in psoriasis. The Journal of Immunology 187(1):490\u2013500. https:\/\/doi.org\/10.4049\/jimmunol.1100123","journal-title":"The Journal of Immunology"},{"issue":"22","key":"2452_CR11","doi-asserted-by":"publisher","first-page":"e130835","DOI":"10.1172\/jci.insight.130835","volume":"4","author":"S Lorscheid","year":"2019","unstructured":"Lorscheid, S., A. M\u00fcller, J. L\u00f6ffler, C. Resch, P. Bucher, and F. C. Kurschus et al. 2019. Keratinocyte-derived I\u03baB\u03b6 drives psoriasis and associated systemic inflammation. JCI Insight 4(22):e130835. https:\/\/doi.org\/10.1172\/jci.insight.130835","journal-title":"JCI Insight"},{"issue":"3","key":"2452_CR12","doi-asserted-by":"publisher","first-page":"255","DOI":"10.1007\/s00109-025-02521-4","volume":"103","author":"L Nardi","year":"2025","unstructured":"Nardi, L., F. Bicker, J. Maier, A. Waisman, and M. J. Schmeisser. 2025. Role of CYLD in brain physiology and pathology. Journal of Molecular Medicine (Berlin Germany 103(3):255\u2013263. https:\/\/doi.org\/10.1007\/s00109-025-02521-4","journal-title":"Journal of Molecular Medicine (Berlin Germany"},{"issue":"6","key":"2452_CR13","doi-asserted-by":"publisher","first-page":"dmm050093","DOI":"10.1242\/dmm.050093","volume":"16","author":"JL Mar\u00edn-Rubio","year":"2023","unstructured":"Mar\u00edn-Rubio, J. L., I. Raote, J. Inns, C. Dobson-Stone, and N. Rajan. 2023. CYLD in health and disease. Disease Models & Mechanisms 16(6):dmm050093. https:\/\/doi.org\/10.1242\/dmm.050093","journal-title":"Disease Models & Mechanisms"},{"key":"2452_CR14","doi-asserted-by":"crossref","unstructured":"Kovalenko, A., C. Chable-Bessia, and G. Cantarella. 2003. The tumour suppressor CYLD negatively regulates NF-kB signalling by deubiquitination.","DOI":"10.1038\/nature01802"},{"issue":"5","key":"2452_CR15","doi-asserted-by":"publisher","first-page":"1063","DOI":"10.1038\/s41375-019-0404-1","volume":"33","author":"H van Andel","year":"2019","unstructured":"van Andel, H., K. A. Kocemba, M. Spaargaren, and S. T. Pals. 2019. Aberrant Wnt signaling in multiple myeloma: Molecular mechanisms and targeting options. Leukemia 33(5):1063\u20131075. https:\/\/doi.org\/10.1038\/s41375-019-0404-1","journal-title":"Leukemia"},{"issue":"8","key":"2452_CR16","doi-asserted-by":"publisher","first-page":"581","DOI":"10.1038\/s41419-024-06972-4","volume":"15","author":"H Ni","year":"2024","unstructured":"Ni, H., M. Chen, D. Dong, Y. Zhou, Y. Cao, and R. Ge et al. 2024. CYLD\/HDAC6 signaling regulates the interplay between epithelial-mesenchymal transition and ciliary homeostasis during pulmonary fibrosis. Cell Death & Disease 15(8):581. https:\/\/doi.org\/10.1038\/s41419-024-06972-4","journal-title":"Cell Death & Disease"},{"issue":"6","key":"2452_CR17","doi-asserted-by":"publisher","first-page":"626","DOI":"10.1038\/s41590-020-0681-x","volume":"21","author":"S Mukherjee","year":"2020","unstructured":"Mukherjee, S., R. Kumar, E. Tsakem Lenou, V. Basrur, D. L. Kontoyiannis, and F. Ioakeimidis et al. 2020. Deubiquitination of NLRP6 inflammasome by cyld critically regulates intestinal inflammation. Nature Immunology 21(6):626\u2013635. https:\/\/doi.org\/10.1038\/s41590-020-0681-x","journal-title":"Nature Immunology"},{"issue":"10","key":"2452_CR18","doi-asserted-by":"publisher","first-page":"1766","DOI":"10.3390\/medicina59101766","volume":"59","author":"NH Giang","year":"2023","unstructured":"Giang, N. H., N. T. K. Lien, D. T. Trang, P. T. Huong, N. H. Hoang, and N. T. Xuan. 2023. Associations of A20, CYLD, Cezanne and JAK2 genes and immunophenotype with psoriasis susceptibility. Medicina (Kaunas Lithuania 59(10):1766. https:\/\/doi.org\/10.3390\/medicina59101766","journal-title":"Medicina (Kaunas Lithuania"},{"issue":"12","key":"2452_CR19","doi-asserted-by":"publisher","first-page":"2498","DOI":"10.1016\/j.jid.2016.07.008","volume":"136","author":"X Xing","year":"2016","unstructured":"Xing, X., Y. Liang, M. K. Sarkar, L. Wolterink, W. R. Swindell, and J. J. Voorhees et al. 2016. IL-17 responses are the dominant inflammatory signal linking Inverse, Erythrodermic, and chronic plaque psoriasis. The Journal of Investigative Dermatology 136(12):2498\u20132501. https:\/\/doi.org\/10.1016\/j.jid.2016.07.008","journal-title":"The Journal of Investigative Dermatology"},{"issue":"1","key":"2452_CR20","doi-asserted-by":"publisher","first-page":"109","DOI":"10.1016\/j.jaci.2016.08.056","volume":"140","author":"A Johnston","year":"2017","unstructured":"Johnston, A., X. Xing, L. Wolterink, D. H. Barnes, Z. Yin, and L. Reingold et al. 2017. IL-1 and IL-36 are dominant cytokines in generalized pustular psoriasis. The Journal of Allergy and Clinical Immunology 140(1):109\u2013120. https:\/\/doi.org\/10.1016\/j.jaci.2016.08.056","journal-title":"The Journal of Allergy and Clinical Immunology"},{"issue":"2","key":"2452_CR21","doi-asserted-by":"publisher","first-page":"199","DOI":"10.1038\/ng.311","volume":"41","author":"RP Nair","year":"2009","unstructured":"Nair, R. P., K. C. Duffin, C. Helms, J. Ding, P. E. Stuart, and D. Goldgar et al. 2009. Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways. Nature Genetics 41(2):199\u2013204. https:\/\/doi.org\/10.1038\/ng.311","journal-title":"Nature Genetics"},{"issue":"6","key":"2452_CR22","doi-asserted-by":"publisher","first-page":"779","DOI":"10.1016\/j.ajhg.2010.10.024","volume":"87","author":"J Ding","year":"2010","unstructured":"Ding, J., J. E. Gudjonsson, L. Liang, P. E. Stuart, Y. Li, and W. Chen et al. 2010. Gene expression in skin and lymphoblastoid cells: Refined statistical method reveals extensive overlap in cis-eQTL signals. American Journal of Human Genetics 87(6):779\u2013789. https:\/\/doi.org\/10.1016\/j.ajhg.2010.10.024","journal-title":"American Journal of Human Genetics"},{"issue":"4","key":"2452_CR23","doi-asserted-by":"publisher","first-page":"e18266","DOI":"10.1371\/journal.pone.0018266","volume":"6","author":"WR Swindell","year":"2011","unstructured":"Swindell, W. R., A. Johnston, S. Carbajal, G. Han, C. Wohn, and J. Lu et al. 2011. Genome-wide expression profiling of five mouse models identifies similarities and differences with human psoriasis. PLoS One 6(4):e18266. https:\/\/doi.org\/10.1371\/journal.pone.0018266","journal-title":"PLoS One"},{"issue":"5","key":"2452_CR24","doi-asserted-by":"publisher","first-page":"453","DOI":"10.1038\/nmeth.3337","volume":"12","author":"AM Newman","year":"2015","unstructured":"Newman, A. M., C. L. Liu, M. R. Green, A. J. Gentles, W. Feng, and Y. Xu et al. 2015. Robust enumeration of cell subsets from tissue expression profiles. Nature Methods 12(5):453\u2013457. https:\/\/doi.org\/10.1038\/nmeth.3337","journal-title":"Nature Methods"},{"issue":"1","key":"2452_CR25","doi-asserted-by":"publisher","first-page":"23848","DOI":"10.1038\/s41598-024-75069-x","volume":"14","author":"Y Zhao","year":"2024","unstructured":"Zhao, Y., L. Wang, X. Zhang, L. Zhang, F. Wei, and S. Li et al. 2024. Identification of neutrophil extracellular traps genes as potential biomarkers in psoriasis based on bioinformatics analysis. Scientific Reports 14(1):23848. https:\/\/doi.org\/10.1038\/s41598-024-75069-x","journal-title":"Scientific Reports"},{"issue":"10","key":"2452_CR26","doi-asserted-by":"publisher","first-page":"659","DOI":"10.1038\/s41419-023-06183-3","volume":"14","author":"L Gao","year":"2023","unstructured":"Gao, L., W. Zhang, X. H. Shi, X. Chang, Y. Han, and C. Liu et al. 2023. The mechanism of linear ubiquitination in regulating cell death and correlative diseases. Cell Death & Disease 14(10):659. https:\/\/doi.org\/10.1038\/s41419-023-06183-3","journal-title":"Cell Death & Disease"},{"key":"2452_CR27","doi-asserted-by":"publisher","DOI":"10.1016\/j.jid.2025.05.006","author":"AA Yurchenko","year":"2025","unstructured":"Yurchenko, A. A., H. Sharkhith, F. Rajabi, S. Bogiatzi, J. Wang, and M. Huber et al. 2025. Integrative molecular analysis of skin tumors from patients with CYLD cutaneous syndrome. The Journal of Investigative Dermatology. https:\/\/doi.org\/10.1016\/j.jid.2025.05.006","journal-title":"The Journal of Investigative Dermatology"},{"issue":"4","key":"2452_CR28","doi-asserted-by":"publisher","first-page":"665","DOI":"10.1016\/j.cell.2006.03.041","volume":"125","author":"R Massoumi","year":"2006","unstructured":"Massoumi, R., K. Chmielarska, K. Hennecke, A. Pfeifer, and R. Fassler. 2006. Cyld inhibits tumor cell proliferation by blocking Bcl-3-dependent NF-kappaB signaling. Cell 125(4):665\u2013677. https:\/\/doi.org\/10.1016\/j.cell.2006.03.041","journal-title":"Cell"},{"issue":"6950","key":"2452_CR29","doi-asserted-by":"publisher","first-page":"793","DOI":"10.1038\/nature01803","volume":"424","author":"E Trompouki","year":"2003","unstructured":"Trompouki, E., E. Hatzivassiliou, T. Tsichritzis, H. Farmer, A. Ashworth, and G. Mosialos. 2003. CYLD is a deubiquitinating enzyme that negatively regulates NF-kappaB activation by TNFR family members. Nature 424(6950):793\u2013796. https:\/\/doi.org\/10.1038\/nature01803","journal-title":"Nature"},{"issue":"1","key":"2452_CR30","doi-asserted-by":"publisher","first-page":"221","DOI":"10.1084\/jem.20082044","volume":"206","author":"R Massoumi","year":"2009","unstructured":"Massoumi, R., S. Kuphal, C. Hellerbrand, B. Haas, P. Wild, and T. Spruss et al. 2009. Down-regulation of CYLD expression by snail promotes tumor progression in malignant melanoma. Journal of Experimental Medicine 206(1):221\u2013232. https:\/\/doi.org\/10.1084\/jem.20082044","journal-title":"Journal of Experimental Medicine"},{"issue":"1","key":"2452_CR31","doi-asserted-by":"publisher","first-page":"25","DOI":"10.1038\/cdd.2009.43","volume":"17","author":"SC Sun","year":"2010","unstructured":"Sun, S. C. 2010. CYLD: A tumor suppressor deubiquitinase regulating NF-kappaB activation and diverse biological processes. Cell Death and Differentiation 17(1):25\u201334. https:\/\/doi.org\/10.1038\/cdd.2009.43","journal-title":"Cell Death and Differentiation"},{"key":"2452_CR32","doi-asserted-by":"publisher","first-page":"771","DOI":"10.1038\/ncomms1776","volume":"3","author":"JH Lim","year":"2012","unstructured":"Lim, J. H., H. Jono, K. Komatsu, C. H. Woo, J. Lee, and M. Miyata et al. 2012. CYLD negatively regulates transforming growth factor-beta-signalling via deubiquitinating Akt. Nature Communications 3:771. https:\/\/doi.org\/10.1038\/ncomms1776","journal-title":"Nature Communications"},{"key":"2452_CR33","doi-asserted-by":"publisher","first-page":"1507989","DOI":"10.3389\/fimmu.2025.1507989","volume":"16","author":"C Schmidt","year":"2025","unstructured":"Schmidt, C., K. Harit, S. Traidl, M. Naumann, T. Werfel, and L. M. Roesner et al. 2025. Ablation of the deubiquitinating enzyme cylindromatosis (CYLD) augments STAT1-mediated M1 macrophage polarization and fosters Staphylococcus aureus control. Frontiers in Immunology 16:1507989. https:\/\/doi.org\/10.3389\/fimmu.2025.1507989","journal-title":"Frontiers in Immunology"},{"issue":"11","key":"2452_CR34","doi-asserted-by":"publisher","first-page":"2637","DOI":"10.1038\/jid.2009.157","volume":"129","author":"T Oudot","year":"2009","unstructured":"Oudot, T., F. Lesueur, M. Guedj, R. de Cid, S. McGinn, and S. Heath et al. 2009. An association study of 22 candidate genes in psoriasis families reveals shared genetic factors with other autoimmune and skin disorders. The Journal of Investigative Dermatology 129(11):2637\u20132645. https:\/\/doi.org\/10.1038\/jid.2009.157","journal-title":"The Journal of Investigative Dermatology"},{"issue":"4","key":"2452_CR35","doi-asserted-by":"publisher","first-page":"854","DOI":"10.1111\/bjd.16083","volume":"178","author":"L Chen","year":"2018","unstructured":"Chen, L., and T. F. Tsai. 2018. HLA-Cw6 and psoriasis. British Journal of Dermatology 178(4):854\u2013862. https:\/\/doi.org\/10.1111\/bjd.16083","journal-title":"British Journal of Dermatology"},{"issue":"8","key":"2452_CR36","doi-asserted-by":"publisher","first-page":"1265","DOI":"10.1136\/gutjnl-2012-303205","volume":"63","author":"I Cleynen","year":"2014","unstructured":"Cleynen, I., E. Vazeille, M. Artieda, H. W. Verspaget, M. Szczypiorska, and M-A. Bringer et al. 2014. Genetic and microbial factors modulating the ubiquitin proteasome system in inflammatory bowel disease. Gut 63(8):1265\u20131274. https:\/\/doi.org\/10.1136\/gutjnl-2012-303205","journal-title":"Gut"},{"issue":"4","key":"2452_CR37","doi-asserted-by":"publisher","first-page":"1519","DOI":"10.1172\/JCI59743","volume":"122","author":"J Daniluk","year":"2012","unstructured":"Daniluk, J., Y. Liu, D. Deng, J. Chu, H. Huang, and S. Gaiser et al. 2012. An NF-\u03baB pathway-mediated positive feedback loop amplifies Ras activity to pathological levels in mice. The Journal of Clinical Investigation 122(4):1519\u20131528. https:\/\/doi.org\/10.1172\/JCI59743","journal-title":"The Journal of Clinical Investigation"},{"issue":"19","key":"2452_CR38","doi-asserted-by":"publisher","first-page":"9453","DOI":"10.1073\/pnas.1821068116","volume":"116","author":"Z Ji","year":"2019","unstructured":"Ji, Z., L. He, A. Regev, and K. Struhl. 2019. Inflammatory regulatory network mediated by the joint action of NF-kB, STAT3, and AP-1 factors is involved in many human cancers. Proceedings of the National Academy of Sciences of the United States of America 116(19):9453\u20139462. https:\/\/doi.org\/10.1073\/pnas.1821068116","journal-title":"Proceedings of the National Academy of Sciences of the United States of America"},{"issue":"2","key":"2452_CR39","doi-asserted-by":"publisher","first-page":"528","DOI":"10.1172\/JCI68101","volume":"124","author":"Y Kagoya","year":"2014","unstructured":"Kagoya, Y., A. Yoshimi, K. Kataoka, M. Nakagawa, K. Kumano, and S. Arai et al. 2014. Positive feedback between NF-\u03baB and TNF-\u03b1 promotes leukemia-initiating cell capacity. The Journal of Clinical Investigation 124(2):528\u2013542. https:\/\/doi.org\/10.1172\/JCI68101","journal-title":"The Journal of Clinical Investigation"},{"issue":"1","key":"2452_CR40","doi-asserted-by":"publisher","first-page":"81","DOI":"10.1038\/s41419-022-04523-3","volume":"13","author":"X Zhou","year":"2022","unstructured":"Zhou, X., Y. Chen, L. Cui, Y. Shi, and C. Guo. 2022. Advances in the pathogenesis of psoriasis: From keratinocyte perspective. Cell Death & Disease 13(1):81. https:\/\/doi.org\/10.1038\/s41419-022-04523-3","journal-title":"Cell Death & Disease"},{"issue":"4","key":"2452_CR41","doi-asserted-by":"publisher","first-page":"301","DOI":"10.1038\/s41419-020-2495-z","volume":"11","author":"J-W Shin","year":"2020","unstructured":"Shin, J-W., M-A. Kwon, J. Hwang, S-J. Lee, J-H. Lee, and H-J. Kim et al. 2020. Keratinocyte transglutaminase 2 promotes CCR6\u2009+\u2009\u03b3\u03b4T-cell recruitment by upregulating CCL20 in psoriatic inflammation. Cell Death & Disease 11(4):301. https:\/\/doi.org\/10.1038\/s41419-020-2495-z","journal-title":"Cell Death & Disease"},{"issue":"11","key":"2452_CR42","doi-asserted-by":"publisher","first-page":"113449","DOI":"10.1016\/j.celrep.2023.113449","volume":"42","author":"J Hao","year":"2023","unstructured":"Hao, J., J. Yu, M. S. Yorek, C-L. Yu, R. M. Pope, and M. S. Chimenti et al. 2023. Keratinocyte FABP5-VCP complex mediates recruitment of neutrophils in psoriasis. Cell Reports 42(11):113449. https:\/\/doi.org\/10.1016\/j.celrep.2023.113449","journal-title":"Cell Reports"},{"issue":"1","key":"2452_CR43","doi-asserted-by":"publisher","first-page":"124","DOI":"10.1007\/s00018-025-05654-4","volume":"82","author":"Y-C Wu","year":"2025","unstructured":"Wu, Y-C., B-H. Su, W-H. Cheng, C-T. Zou, E. T. H. Yeh, and F-M. Yang. 2025. CYLD links the TRAF6\/sNASP axis to TLR4 signaling in sepsis-induced acute lung injury. Cellular and Molecular Life Sciences: CMLS 82(1):124. https:\/\/doi.org\/10.1007\/s00018-025-05654-4","journal-title":"Cellular and Molecular Life Sciences: CMLS"},{"issue":"6","key":"2452_CR44","doi-asserted-by":"publisher","first-page":"1475","DOI":"10.1084\/jem.20062694","volume":"204","author":"WW Reiley","year":"2007","unstructured":"Reiley, W. W., W. Jin, A. J. Lee, A. Wright, X. Wu, and E. F. Tewalt et al. 2007. Deubiquitinating enzyme CYLD negatively regulates the ubiquitin-dependent kinase Tak1 and prevents abnormal T cell responses. Journal of Experimental Medicine 204(6):1475\u20131485. https:\/\/doi.org\/10.1084\/jem.20062694","journal-title":"Journal of Experimental Medicine"},{"issue":"18","key":"2452_CR45","doi-asserted-by":"publisher","first-page":"2847","DOI":"10.1093\/bioinformatics\/btw313","volume":"32","author":"Z Gu","year":"2016","unstructured":"Gu, Z., R. Eils, and M. Schlesner. 2016. Complex heatmaps reveal patterns and correlations in multidimensional genomic data. Bioinformatics (Oxford England 32(18):2847\u20132849. https:\/\/doi.org\/10.1093\/bioinformatics\/btw313","journal-title":"Bioinformatics (Oxford England"},{"issue":"30","key":"2452_CR46","doi-asserted-by":"publisher","first-page":"4280","DOI":"10.1002\/sim.5515","volume":"31","author":"S Senn","year":"2012","unstructured":"Senn, S., N. Holford, and H. Hockey. 2012. The ghosts of departed quantities: Approaches to dealing with observations below the limit of quantitation. Statistics in Medicine 31(30):4280\u20134295. https:\/\/doi.org\/10.1002\/sim.5515","journal-title":"Statistics in Medicine"},{"key":"2452_CR47","doi-asserted-by":"publisher","first-page":"40508","DOI":"10.1038\/srep40508","volume":"7","author":"Z Chen","year":"2017","unstructured":"Chen, Z., A. Huang, J. Sun, T. Jiang, FX-F. Qin, and A. Wu. 2017. Inference of immune cell composition on the expression profiles of mouse tissue. Scientific Reports 7:40508. https:\/\/doi.org\/10.1038\/srep40508","journal-title":"Scientific Reports"}],"container-title":["Inflammation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/link.springer.com\/article\/10.1007\/s10753-026-02452-3","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1007\/s10753-026-02452-3.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1007\/s10753-026-02452-3.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,2,9]],"date-time":"2026-02-09T14:11:19Z","timestamp":1770646279000},"score":1,"resource":{"primary":{"URL":"https:\/\/link.springer.com\/10.1007\/s10753-026-02452-3"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,1,20]]},"references-count":47,"journal-issue":{"issue":"1","published-online":{"date-parts":[[2026,12]]}},"alternative-id":["2452"],"URL":"https:\/\/doi.org\/10.1007\/s10753-026-02452-3","relation":{"has-preprint":[{"id-type":"doi","id":"10.21203\/rs.3.rs-7849804\/v1","asserted-by":"object"}]},"ISSN":["1573-2576"],"issn-type":[{"value":"1573-2576","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,1,20]]},"assertion":[{"value":"13 October 2025","order":1,"name":"received","label":"Received","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"17 December 2025","order":2,"name":"revised","label":"Revised","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"7 January 2026","order":3,"name":"accepted","label":"Accepted","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"20 January 2026","order":4,"name":"first_online","label":"First Online","group":{"name":"ArticleHistory","label":"Article History"}},{"order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Declarations"}},{"value":"This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the by the Institutional Animal Care and Use Committee of Chinese PLA General Hospital.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics Approval"}},{"value":"The authors declare no competing interests.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"57"}}