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Expression and modulation by cytokines of the intercellular adhesion molecule‐1 (ICAM‐1) in human central nervous system tumor cell cultures
Author(s) -
Guarini Ludovico,
Temponi Massimo,
Bruce Jeffrey N.,
Bollon Arthur P.,
Duigou Gregory J.,
Moulton Thomas A.,
Ferrone Soldano,
Fisher Paul B.
Publication year - 1990
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910460616
Subject(s) - biology , tumor necrosis factor alpha , intercellular adhesion molecule 1 , cell culture , cell adhesion molecule , immune system , icam 1 , cytokine , pathology , microbiology and biotechnology , cancer research , immunology , medicine , genetics
The intercellular adhesion molecule (ICAM‐1) has been shown to be important in interactions involying cells of the immune system and to be upregulated in a number of cell culture systems by cytokines, including immune interferon (IFN‐γ) and tumor necrosis factor‐alpha (TNF‐α). In the present study, we have determined by fluorescence‐activated cell sorter (FACS) analysis and the anti‐ICAM‐I monoclonal antibody (MAb) CL203.4 the base‐line expression of ICAM‐I and its modulation by recombinant IFN‐β, IFN‐γ and TNF‐α in early passage (< 15) human central nervous system (CNS) tumor‐derived cell cultures. These cultures were established from various malignancies, including glioblastoma multiforme (GBM), astrocytoma (AST), ganglioglioma, medulloblastoma, meningioma and a pineal tumor. ICAM‐I expression was highest in the GBM‐ and AST‐derived cell cultures and was lowest in the ganglioglioma and normal pineal cell cultures. Variable ICAM‐I expression was found, however, in tumors of the same histological group. In several cell cultures the variable expression observed by FACS was substantiated by the intensity of the molecular species immunoprecipitated by the anti‐ICAM‐I MAb CL203.4 from these cells. All the cell cultures displayed variable but consistent increases in ICAM‐I expression following treatment with IFN‐γ or TNF‐α. In general, the degree of increase in ICAM‐I expression was greatest in cultures exposed to TNF‐α. Upregulation of ICAM‐I expression in an established glioblastoma multiforme cell line was of greater magnitude and more rapid following TNF‐α treatment (within 2 to 3 hr) than exposure to IFN‐γ (by 24 hr). In several cultures, IFN‐β also increased ICAM‐I expression and enhanced the increase induced by TNF‐α. The results of the present study indicate that variable expression of ICAM‐I is a common property of early passage cultures of CNS tumors and recombinant interferons and TNF‐α can differentially upregulate ICAM‐I expression in these CNS tumor cell cultures.