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Interleukin 4 and Tumour Necrosis Factor α Induce Different Adhesion Pathways in Endothelial Cells for the Binding of Peripheral Blood Lymphocytes
Author(s) -
GALÉA P.,
LEBRANCHU Y.,
THIBAULT G.,
BARDOS P.
Publication year - 1992
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1992.tb03226.x
Subject(s) - cell adhesion molecule , adhesion , tumor necrosis factor alpha , cell adhesion , icam 1 , microbiology and biotechnology , chemistry , interleukin , cytokine , immunology , biology , organic chemistry
We demonstrated that tumour necrosis factor α (TNF‐α) and interleukin 4 (IL‐4) increased endothelial cell (EC) adhesiveness for peripheral blood lymphocytes (PBL) by promoting transcription and protein synthesis. Theo different kinetics observed with TNF‐α and IL‐4 suggest the involvement of different adhesion molecules. Blocking adhesion assays and immunofluorescence analysis showed that PBL adhesion to endothelial cells involves different pair adhesion molecules. Whereas IL‐4 promoted an LFA‐1‐dependent/ICAM‐1‐independent adhesion pathway on EC, TNF‐α stimulated an LFA‐1‐dependent/ICAM‐1‐dependent adhesion pathway on EC. In conttast. VLA‐4/VCAM‐1 molecules were involved in PBL adhesion both to IL‐4 and to TNF‐α‐stimulated EC. Finally, we found that a CD2‐dependent/LFA‐3‐independent adhesion pathway was mainly involved in IL‐4‐stimulated EC.