Tumor-driven matrix invasion by infiltrating lymphocytes: Involvement of the α1 integrin I-domain

Research output: Contribution to journalArticlepeer-review

Abstract

Here we show that tumor cells (TC) from renal cancers regulate the migratory properties of autologous tumor-infiltrating lymphocytes (TIL), enhancing their ability to invade the extracellular matrix. A similar effect is exerted by human recombinant macrophage chemotactic protein 1 (MOP-1) and IL-8, chemokines known to increase T lymphocyte migration both across vascular endothelium and subendothelial matrix. We found that TC freshly derived from renal cell carcinoma surgical specimens constitutively secrete both IL-8 and MOP-1 and that TIL express both specific receptors. TIL matrix invasion elicited by TC is inhibited by the addition of neutralizing antisera specific for IL-8 and MCP-1, demonstrating the direct relationship between chemokine release by TC and TIL invasion. Of note, TIL invasion of the extracellular matrix requires the α1 integrin, which acts through its I-domain that is up-regulated upon culture with MCP-1 and IL-8. Collectively, these findings suggest that TC may actively recruit TIL via the release of chemotactic factors that enhance an α1 integrin-mediated pathway of matrix invasion.

Original languageEnglish
Pages (from-to)2530-2536
Number of pages7
JournalEuropean Journal of Immunology
Volume28
Issue number8
DOIs
Publication statusPublished - Aug 1998

Keywords

  • Adhesion molecule
  • Chemokine
  • Extracellular matrix
  • Integrin
  • Tumor-infiltrating lymphocyte

ASJC Scopus subject areas

  • Immunology

Fingerprint Dive into the research topics of 'Tumor-driven matrix invasion by infiltrating lymphocytes: Involvement of the α1 integrin I-domain'. Together they form a unique fingerprint.

Cite this