Adhesion of tumoricidal eosinophils to MCA-38 colon adenocarcinoma cells involves protein tyrosine kinase activation and is diminished by elevated cyclic AMP in the effector cell

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Résumé

Although eosinophils have been implicated in immune responses to certain types of tumors, the mechanisms of anti-tumor activity by eosinophils are poorly understood. We show here that mouse eosinophils kill allogeneic MCA- 38 colon adenocarcinoma cells in the absence of specific antibody. Eosinophil adhesion to MCA-38 monolayers occurred within 15 min and plateaued at 90 min. Although mouse eosinophils express α(L) (CD11a), α(M) (CD11b), and α4 (CD49d) integrin chains, blocking antibody studies revealed that these molecules are not involved in eosinophil binding to MCA-38 cells. Adhesion was also fibronectin-independent. Binding was inhibited when eosinophils, but not MCA-38 cells, were pretreated with methyl 2,5-dihydroxycinnamate (MDHC), a selective inhibitor of protein tyrosine kinases, or 8-Br-cAMP-Na, a cell- permeable cyclic AMP analogue. Adhesion was unaffected by calphostin C, a specific inhibitor of protein kinase C, and wortmannin, a selective inhibitor of phosphatidylinositol 3-kinases.

Langue d'origineEnglish
Pages (de-à)1305-1311
Nombre de pages7
JournalInternational Journal of Oncology
Volume13
Numéro de publication6
DOI
Statut de publicationPublished - déc. 1998

ASJC Scopus Subject Areas

  • Oncology
  • Cancer Research

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't

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