loading page

sNASP mutation aggravates to the TLR4-mediated inflammation in SLE by TAK1 pathway
  • +4
  • Yatao Bao,
  • Meng Lian,
  • Yong Chen,
  • Xiaotian Gu,
  • Kunyu Cao,
  • Xiaoping Du,
  • Ji-Yu Ju
Yatao Bao
Weifang Medical University
Author Profile
Meng Lian
Weifang Medical University
Author Profile
Yong Chen
Weifang Medical University
Author Profile
Xiaotian Gu
Weifang Medical University
Author Profile
Kunyu Cao
Weifang Medical University
Author Profile
Xiaoping Du
The Second Affiliated Hospital of Weifang Medical University
Author Profile
Ji-Yu Ju
Weifang Medical University

Corresponding Author:[email protected]

Author Profile

Abstract

Genetic factors play an important role in the pathogenesis of systemic lupus erythematosus, and abnormal TLR signaling pathways are closely related to the onset of SLE. In previous studies, we found that the mutant somatic nuclear autoantigenic sperm protein (sNASP) gene in the mouse lupus susceptibility locus Sle2 can promote the development of lupus model mice, but the mechanism is still unclear. Here, we stimulated mouse peritoneal macrophages with different concentrations of LPS. The results showed that sNASP gene mutations can promote the response of the TLR4-TAK1 signaling pathway, but have no significant effect on the TLR4-TBK1 signaling pathway. sNASP mutations enhanced TLR4-mediated NF-KB and MAPK activation and IL-6, TNF secretion in murine peritoneal macrophages. Collectively, our study revealed the impact of sNASP gene mutation on the sensitivity of TLR4 receptors in mouse peritoneal macrophages and shed light on potential mechanisms underlying inflammation in autoimmune diseases.