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Role of Enhanced Cellular Adhesion in IL‐6‐Augmented Lymphokine‐Activated Killer‐Cell Function
Author(s) -
IHO S.,
SHAU H.
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.tb03366.x
Subject(s) - lymphokine activated killer cell , cytolysis , lymphokine , interleukin 2 , cytotoxic t cell , cytotoxicity , aldesleukin , immunology , chemistry , biology , microbiology and biotechnology , interleukin 21 , in vitro , immune system , biochemistry
The authors demonstrated previously that a short‐term treatment with IL‐6 of lymphokine‐activated killer (LAK) cells produces an increase in cytotoxic activity of CD56 + /CD3 − effector cells generated from human PBL as well as from human thymocytes. In the study described here, the mechanisms by which IL‐6 enhances LAK cytotoxicity were examined. Like untreated LAK cells, IL‐6‐treated LAK cells require Ca ++ to initiate cytolysis. However, IL‐6 treatment of LAK cells does not alter the rate of programming for lysis. Instead, IL‐6 increases target‐binding capacity of CD56 + /CD3 − LAK cells in association with the increased cytotoxicity. Similar to target‐binding of untreated LAK cells, the binding between IL‐6‐treated LAK cells and target cells is dependent on Mg ++ . Cellular adhesion molecules (CAM), CD1 la‐c, CD18. CD54. CD56, CD58 and CD2 (T11, epitope). are up‐regulated in LAK cells by culture with IL‐2. Among MoAbs to these CAMs. only Abs to CD11a/CD18 (LFA‐1) and CD54 (ICAM‐1) decrease both target‐binding and cytolysis by LAK cells. IL‐6 treatment changes neither the proportion nor the intensity of CAM positive cells. However, MoAbs to CD11a/CD18 and CD54 reduce both target‐conjugation and cytotoxicity of IL‐6‐enhanced LAK cells to the same level as control LAK cells treated with the MoAbs. IL‐6‐enhanced LAK functions (both target‐conjugation and target‐lysis) are not abrogated by MoAbs to other CAM which do not inhibit standard LAK functions. These results indicate that IL‐6 up‐regulates cellular events mediated by CD11a/CD18 and CD54 molecules which are involved in standard LAK functions. These events may result in activation of lytic efieclor cells, associated with an increase in target‐binding and an increase in cytotoxicity.