期刊
ARCHIVES OF VIROLOGY
卷 166, 期 4, 页码 1035-1045出版社
SPRINGER WIEN
DOI: 10.1007/s00705-020-04933-8
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资金
- National Natural Sciences Foundation of China [81971943, 81772196, 31470264, 81271820, 30870789, 30300117]
- Stanley Foundation from the Stanley Medical Research Institute (SMRI), United States [06R-1366]
- Medical Science Advancement Program (Basic Medical Sciences) of Wuhan University [TFJC 2018002]
The study revealed that HERV-W env upregulates the expressions of TNF-alpha and IL-10 by inhibiting the production of MyD88s in glial cells. This immune pathogenesis mechanism involving TLR4 and MyD88 sheds light on the role of HERV-W env in neuropsychiatric disorders.
Human endogenous retrovirus W family envelope protein (HERV-W env) is associated with several neurological and psychiatric disorders, including multiple sclerosis (MS) and schizophrenia. Clinical studies have demonstrated a common link between inflammatory abnormalities and HERV-W env in neuropsychiatric diseases. Nonetheless, the molecular mechanisms by which HERV-W env mediates neuroinflammation are still unclear. In this study, we found that HERV-W env significantly increased the mRNA and protein levels of TNF-alpha and IL-10 in U251 and A172 cells. HERV-W env also induced a notable increase in Toll-like receptor 4 (TLR4). Knockdown of TLR4 impaired the expressions of TNF-alpha and IL-10 induced by HERV-W env. Overexpression of HERV-W env led to the upregulation of MyD88 but caused a decrease in MyD88s. MyD88s overexpression suppressed the expressions of TNF-alpha and IL-10 induced by HERV-W env. These findings indicate that HERV-W env upregulates the expressions of IL-10 and TNF-alpha by inhibiting the production of MyD88s in glial cells. This work sheds light on the immune pathogenesis of HERV-W env in neuropsychiatric disorders.
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