Downregulation of T cell immunoglobulin and mucin protein 3 in the pathogenesis of intracranial aneurysm

Inflammation. 2015 Feb;38(1):368-74. doi: 10.1007/s10753-014-0040-x.

Abstract

Evidence has shown that inflammation acts as a critical contributor to the pathogenesis of intracranial aneurysm (IA), a potentially devastating clinical problem. T cell immunoglobulin and mucin protein 3 (Tim-3) is a negative regulatory molecule and plays important roles in the inflammation process. In the current study, we investigated the expression of Tim-3 and its correlation with tumor necrosis factor alpha (TNF-α) in IA patients. Data showed that both messenger RNA (mRNA) level and protein level of Tim-3 were significantly decreased in CD4+ T cells and CD8+ T cells from IA patients than from healthy controls (P < 0.001). However, expression of Tim-3 was not altered in monocytes between patients and healthy donors. Further analyses revealed that patients with ruptured aneurysm had significantly lower level of Tim-3 in CD8+ T cells than those with un-ruptured aneurysm. In addition, a negative correlation between serum level of TNF-α and the expression of Tim-3 in CD4+ T cells was observed in IA patients. Similar correlation was also identified in CD8+ T cells from IA patients. Our study suggests that Tim-3 may participate in the development and progression of IA by probably its negative regulation on TNF-α.

MeSH terms

  • Adult
  • Aged
  • CD4-Positive T-Lymphocytes / metabolism*
  • CD8-Positive T-Lymphocytes / metabolism*
  • Down-Regulation / physiology*
  • Female
  • Hepatitis A Virus Cellular Receptor 2
  • Humans
  • Intracranial Aneurysm / diagnosis*
  • Intracranial Aneurysm / metabolism*
  • Male
  • Membrane Proteins / biosynthesis*
  • Middle Aged

Substances

  • HAVCR2 protein, human
  • Hepatitis A Virus Cellular Receptor 2
  • Membrane Proteins