Eine Plattform für die Wissenschaft: Bauingenieurwesen, Architektur und Urbanistik
Eine Plattform für die Wissenschaft: Bauingenieurwesen, Architektur und Urbanistik
Cutaneous Calcium/Calmodulin‐Dependent Protein Kinase II‐γ–Positive Sympathetic Nerves Secreting Norepinephrine Dictate Psoriasis
https://orcid.org/0000-0002-2138-5953
https://orcid.org/0000-0002-9581-0502
https://orcid.org/0000-0002-6789-661X
https://orcid.org/0000-0001-7084-6376
https://orcid.org/0000-0003-2347-6493
https://orcid.org/0000-0003-0123-1065
https://orcid.org/0000-0002-8344-4461
https://orcid.org/0000-0002-8499-5353
AbstractCutaneous sympathetic nerve is a crucial part of neuropsychiatric factors contributing to skin immune response, but its role in the psoriasis pathogenesis remains unclear. It is found that cutaneous calcium/calmodulin‐dependent protein kinase II‐γ (CAMK2γ), expressed mainly in sympathetic nerves, is activated by stress and imiquimod in mouse skin. Camk2g‐deficient mice exhibits attenuated imiquimod‐induced psoriasis‐like manifestations and skin inflammation. CaMK2γ regulates dermal γδT‐cell interleukin‐17 production in imiquimod‐treated mice, dependent on norepinephrine production following cutaneous sympathetic nerve activation. Adrenoceptor β1, the primary skin norepinephrine receptor, colocalises with γδT cells. CaMK2γ aggravates psoriasiform inflammation via sympathetic nerve–norepinephrine–γδT cell–adrenoceptor β1–nuclear factor‐κB and –p38 axis activation. Application of alcaftadine, a small‐molecule CaMK2γ inhibitor, relieves imiquimod‐induced psoriasis‐like manifestations in mice. This study reveals the mechanisms of sympathetic‐nervous‐system regulation of γδT‐cell interleukin‐17 secretion, and provides insight into neuropsychiatric factors dictating psoriasis pathogenesis and new potential targets for clinical psoriasis treatment.
Cutaneous Calcium/Calmodulin‐Dependent Protein Kinase II‐γ–Positive Sympathetic Nerves Secreting Norepinephrine Dictate Psoriasis
https://orcid.org/0000-0002-2138-5953
https://orcid.org/0000-0002-9581-0502
https://orcid.org/0000-0002-6789-661X
https://orcid.org/0000-0001-7084-6376
https://orcid.org/0000-0003-2347-6493
https://orcid.org/0000-0003-0123-1065
https://orcid.org/0000-0002-8344-4461
https://orcid.org/0000-0002-8499-5353
AbstractCutaneous sympathetic nerve is a crucial part of neuropsychiatric factors contributing to skin immune response, but its role in the psoriasis pathogenesis remains unclear. It is found that cutaneous calcium/calmodulin‐dependent protein kinase II‐γ (CAMK2γ), expressed mainly in sympathetic nerves, is activated by stress and imiquimod in mouse skin. Camk2g‐deficient mice exhibits attenuated imiquimod‐induced psoriasis‐like manifestations and skin inflammation. CaMK2γ regulates dermal γδT‐cell interleukin‐17 production in imiquimod‐treated mice, dependent on norepinephrine production following cutaneous sympathetic nerve activation. Adrenoceptor β1, the primary skin norepinephrine receptor, colocalises with γδT cells. CaMK2γ aggravates psoriasiform inflammation via sympathetic nerve–norepinephrine–γδT cell–adrenoceptor β1–nuclear factor‐κB and –p38 axis activation. Application of alcaftadine, a small‐molecule CaMK2γ inhibitor, relieves imiquimod‐induced psoriasis‐like manifestations in mice. This study reveals the mechanisms of sympathetic‐nervous‐system regulation of γδT‐cell interleukin‐17 secretion, and provides insight into neuropsychiatric factors dictating psoriasis pathogenesis and new potential targets for clinical psoriasis treatment.
Cutaneous Calcium/Calmodulin‐Dependent Protein Kinase II‐γ–Positive Sympathetic Nerves Secreting Norepinephrine Dictate Psoriasis
https://orcid.org/0000-0002-2138-5953
https://orcid.org/0000-0002-9581-0502
https://orcid.org/0000-0002-6789-661X
https://orcid.org/0000-0001-7084-6376
https://orcid.org/0000-0003-2347-6493
https://orcid.org/0000-0003-0123-1065
https://orcid.org/0000-0002-8344-4461
https://orcid.org/0000-0002-8499-5353
AbstractCutaneous sympathetic nerve is a crucial part of neuropsychiatric factors contributing to skin immune response, but its role in the psoriasis pathogenesis remains unclear. It is found that cutaneous calcium/calmodulin‐dependent protein kinase II‐γ (CAMK2γ), expressed mainly in sympathetic nerves, is activated by stress and imiquimod in mouse skin. Camk2g‐deficient mice exhibits attenuated imiquimod‐induced psoriasis‐like manifestations and skin inflammation. CaMK2γ regulates dermal γδT‐cell interleukin‐17 production in imiquimod‐treated mice, dependent on norepinephrine production following cutaneous sympathetic nerve activation. Adrenoceptor β1, the primary skin norepinephrine receptor, colocalises with γδT cells. CaMK2γ aggravates psoriasiform inflammation via sympathetic nerve–norepinephrine–γδT cell–adrenoceptor β1–nuclear factor‐κB and –p38 axis activation. Application of alcaftadine, a small‐molecule CaMK2γ inhibitor, relieves imiquimod‐induced psoriasis‐like manifestations in mice. This study reveals the mechanisms of sympathetic‐nervous‐system regulation of γδT‐cell interleukin‐17 secretion, and provides insight into neuropsychiatric factors dictating psoriasis pathogenesis and new potential targets for clinical psoriasis treatment.
Cutaneous Calcium/Calmodulin‐Dependent Protein Kinase II‐γ–Positive Sympathetic Nerves Secreting Norepinephrine Dictate Psoriasis
Advanced Science
Yu, Yafen (Autor:in) / Chen, Weiwei (Autor:in) / Li, Bao (Autor:in) / Li, Zhuo (Autor:in) / Wang, Yirui (Autor:in) / Mao, Yiwen (Autor:in) / Fan, Wencheng (Autor:in) / Bai, Yuanming (Autor:in) / Hu, Hongbo (Autor:in) / Zhen, Qi (Autor:in)
Advanced Science ; 11
01.06.2024
Aufsatz (Zeitschrift)
Elektronische Ressource
Englisch
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