1. Academic Validation
  2. Selenoprotein K Is Essential for the Migration and Phagocytosis of Immature Dendritic Cells

Selenoprotein K Is Essential for the Migration and Phagocytosis of Immature Dendritic Cells

  • Antioxidants (Basel). 2022 Jun 27;11(7):1264. doi: 10.3390/antiox11071264.
Huan Xia 1 2 3 Yongmei Wang 1 2 Jie Dai 1 2 Xin Zhang 1 2 Jun Zhou 4 5 Zhu Zeng 1 2 Yi Jia 1 2
Affiliations

Affiliations

  • 1 Key Laboratory of Infectious Immune and Antibody Engineering of Guizhou Province, Cellular Immunotherapy Engineering Research Center of Guizhou Province, School of Biology and Engineering/School of Basic Medical Sciences, Guizhou Medical University, Guiyang 550025, China.
  • 2 Immune Cells and Antibody Engineering Research Center of Guizhou Province, Key Laboratory of Biology and Medical Engineering, Guizhou Medical University, Guiyang 550025, China.
  • 3 Department of Pathology, Guizhou Qiannan People's Hospital, Qiannan 558000, China.
  • 4 Hubei Key Laboratory of Bioinorganic Chemistry & Materia Medica, Hubei Engineering Research Center for Biomaterials and Medical Protective Materials, Key Laboratory of Material Chemistry for Energy Conversion and Storage, Ministry of Education, School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, 1037 Luoyu Road, Wuhan 430074, China.
  • 5 Shenzhen Huazhong University of Science and Technology Research Institute, 9 Yuexing Third Road, Shenzhen 518057, China.
Abstract

Selenoprotein K (SELENOK) is an endoplasmic reticulum stress (ERS)-regulated protein required for the calcium (CA2+) flux-mediated migration of T cells and neutrophils, and the migration and phagocytosis of macrophages and microglia. However, the effect of SELENOK on the regulation of the immune function of dendritic cells (DCs), including immature DCs (imDCs) and mature DCs (mDCs), is still unclear. In this study, imDCs prepared from SELENOK knockout mice were used to evaluate the effect of SELENOK on the migration and phagocytosis of imDCs. The results showed that ERS-induced downregulation of imDCs phenotypic markers led to a reduction in Ras homolog gene family member A (RhoA)-dependent migration and enhanced CA2+/CD205-mediated phagocytosis. SELENOK deficiency-induced upregulation of selenoprotein S (SELENOS) attenuated ERS levels in imDCs. An increase in CA2+ levels resulted in increased migration and decreased phagocytosis with or without ERS conditions. The migration was RhoA-dependent, and CA2+ or CD205 was associated with regulating phagocytosis in imDCs. Our study found that SELENOK is required for imDC migration and phagocytosis.

Keywords

dendritic cells; endoplasmic reticulum stress; selenoprotein K.

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