Cutting edge: Combined treatment of TNF-α and IFN-γ causes redistribution of junctional adhesion molecule in human endothelial cells

Harunobu Ozaki, Kenji Ishii, Hisanori Horiuchi, Hidenori Arai, Takahiro Kawamoto, Katsuya Okawa, Akihiro Iwamatsu, Toru Kita

Research output: Contribution to journalArticlepeer-review

257 Citations (Scopus)

Abstract

Proinflammatory cytokines such as TNF-α and IFN-γ induce cell adhesion molecules in endothelial cells and promote transmigration of leukocytes across endothelial cells. However, when those two were administered together, leukocyte transmigration paradoxically decreased. We cloned a human and bovine homologue of the junctional adhesion molecule (JAM), a novel molecule at the tight junction, and examined the effects of proinflammatory cytokines on JAM in HUVECs. The combined treatment of TNF-α plus IFN-γ caused a disappearance of JAM from intercellular junctions. However, flow cytometry, cell ELISA, and subcellular fractionation analysis demonstrated that the amount of JAM was ant reduced. This suggested that JAM changed its distribution in response to proinflammatory cytokine. This redistribution or JAM might be involved in a decrease in transendothelial migration of leukocytes at inflammatory sites.

Original languageEnglish
Pages (from-to)553-557
Number of pages5
JournalJournal of Immunology
Volume163
Issue number2
Publication statusPublished - 1999 Jul 15
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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