Calcium/calmodulin-dependent protein kinase IV promotes imiquimod-induced psoriatic inflammation via macrophages and keratinocytes in mice

Liang Yong, Yafen Yu, Bao Li, Huiyao Ge, Qi Zhen, Yiwen Mao, Yanxia Yu, Lu Cao, Ruixue Zhang, Zhuo Li, Yirui Wang, Wencheng Fan, Chang Zhang, Daiyue Wang, Sihan Luo, Yuanming Bai, Shirui Chen, Weiwei Chen, Miao Liu, Jijia Shen and Liangdan Sun ()
Additional contact information
Liang Yong: the First Affiliated Hospital of Anhui Medical University
Yafen Yu: the First Affiliated Hospital of Anhui Medical University
Bao Li: Anhui Medical University
Huiyao Ge: the First Affiliated Hospital of Anhui Medical University
Qi Zhen: the First Affiliated Hospital of Anhui Medical University
Yiwen Mao: the First Affiliated Hospital of Anhui Medical University
Yanxia Yu: the First Affiliated Hospital of Anhui Medical University
Lu Cao: the First Affiliated Hospital of Anhui Medical University
Ruixue Zhang: the First Affiliated Hospital of Anhui Medical University
Zhuo Li: the First Affiliated Hospital of Anhui Medical University
Yirui Wang: the First Affiliated Hospital of Anhui Medical University
Wencheng Fan: the First Affiliated Hospital of Anhui Medical University
Chang Zhang: the First Affiliated Hospital of Anhui Medical University
Daiyue Wang: the First Affiliated Hospital of Anhui Medical University
Sihan Luo: the First Affiliated Hospital of Anhui Medical University
Yuanming Bai: the First Affiliated Hospital of Anhui Medical University
Shirui Chen: the First Affiliated Hospital of Anhui Medical University
Weiwei Chen: the First Affiliated Hospital of Anhui Medical University
Miao Liu: Anhui Medical University
Jijia Shen: Anhui Medical University
Liangdan Sun: the First Affiliated Hospital of Anhui Medical University

Nature Communications, 2022, vol. 13, issue 1, 1-16

Abstract: Abstract CaMK4 has an important function in autoimmune diseases, and the contribution of CaMK4 in psoriasis remains obscure. Here, we show that CaMK4 expression is significantly increased in psoriatic lesional skin from psoriasis patients compared to healthy human skin as well as inflamed skin from an imiquimod (IMQ)-induced mouse model of psoriasis compared to healthy mouse skin. Camk4-deficient (Camk4−/−) mice treated with IMQ exhibit reduced severity of psoriasis compared to wild-type (WT) mice. There are more macrophages and fewer IL-17A+γδ TCR+ cells in the skin of IMQ-treated Camk4−/− mice compared to IMQ-treated WT mice. CaMK4 inhibits IL-10 production by macrophages, thus allowing excessive psoriatic inflammation. Deletion of Camk4 in macrophages alleviates IMQ-induced psoriatic inflammation in mice. In keratinocytes, CaMK4 inhibits apoptosis as well as promotes cell proliferation and the expression of pro-inflammatory genes such as S100A8 and CAMP. Taken together, these data indicate that CaMK4 regulates IMQ-induced psoriasis by sustaining inflammation and provides a potential target for psoriasis treatment.

Date: 2022
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DOI: 10.1038/s41467-022-31935-8

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