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Murine Endothelial Cell Line Cells, F‐2: Interaction with Leukocytes and Cytokines Production
Author(s) -
Maruyama Hidenori,
Toda Kenichi,
Uno Kazuko,
Miyake Kensuke,
Matsushima Koji,
Yamamoto Kazuo,
Mori Kazuhiro J.,
Masuda Tohru
Publication year - 1993
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1993.tb01721.x
Subject(s) - biology , lymphocyte function associated antigen 1 , vcam 1 , microbiology and biotechnology , antigen , cell adhesion molecule , chemotaxis , cell adhesion , icam 1 , intercellular adhesion molecule 1 , endothelial stem cell , tumor necrosis factor alpha , cell culture , cell–cell interaction , cytokine , immunology , in vitro , cell , biochemistry , receptor , genetics
Flowcytometry demonstrated that murine endothelial cell line F‐2 expresses MHC class I antigen, FcR II, Mac‐1 and vascular cell adhesion molecule‐1 (VCAM‐1), but not intercellular adhesion molecule‐1 (ICAM‐1) and class II antigen. However, co‐culturing with TNF‐α for 24 hr resulted in the increased expression of ICAM‐1, and the decreased expression of VCAM‐1. IL‐1α and IFN‐γ exerted this regulatory effect on VCAM‐1 but not on ICAM‐1. T (Con A blast) and B (LPS blast) cells adhered to F‐2 cells at almost equal levels, and the adhesion was enhanced 20 to 50% when the cells were precultured with TNF‐α for 24 hr. The inhibition assay using either (anti‐ICAM‐1 + anti‐LFA‐1, lymphocyte function‐associated antigen‐1) or (anti‐VCAM‐1 + anti‐VLA‐4, very late antigen‐4) mAbs demonstrated that the ICAM‐1 system was utilized more preferentially by T than B blasts when F‐2 cells were stimulated with TNF‐α, and the VCAM‐1 system was vice versa under the unstimulated and stimulated conditions. Granulocytes also adhered to F‐2 cells, but no mAbs could inhibit the adhesion. Although F‐2 cells produced a considerable amount of IL‐6, GM‐CSF and neutrophil chemotactic activity, a 24 hr incubation with TNF‐α resulted in an increase of 12 fold in IL‐6 and 3 fold in neutrophil chemotactic activity production.