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Human NK Cells Expressing α4β1/β7 Adhere to VCAM‐1 Without Preactivation
Author(s) -
PINOLA M,
SAKSELA E.,
TIlSALA S.,
RENKONEN R.
Publication year - 1994
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.1365-3083.1994.tb03351.x
Subject(s) - vcam 1 , neural cell adhesion molecule , microbiology and biotechnology , effector , cell adhesion , adhesion , stimulation , cell adhesion molecule , cytotoxic t cell , co stimulation , biology , cell , cd3 , interleukin 21 , t cell , immune system , chemistry , immunology , icam 1 , cd8 , cd28 , in vitro , neuroscience , biochemistry , organic chemistry
The authors demonstrate that resting CD56 + /CD3 − NK cell adhesion to the endothelial VCAM‐1 is over three‐fold higher than CD56 − /CD3 + T‐cell adhesion. T‐cell, but not NK‐cell adhesion, to VCAM‐1 is enhanced significantly by stimulation. The expression of VCAM‐I receptor subunits α4 and β1 on both effector cells remains unchanged upon stimulation. A subpopulation of NK cells, as well as of T cells, was found to express β7, whose expression was not altered upon stimulation. The authors conclude that the adhesive properties of the same receptor structures on these distinct cell populations are regulated in a different manner, according to the specific functions of the effector cells of the immune system.