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Up‐ and down‐regulation of human lymphokine (IL‐2)‐activated killer cell induction by monocytes, depending on their functional state
Author(s) -
Nil Akihiko,
Sone Saburo,
Utsugi Teruhiro,
Yanagawa Hiroaki,
Ogura Takeshi
Publication year - 1988
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.2910410108
Subject(s) - lymphokine activated killer cell , lymphokine , monocyte , tumor necrosis factor alpha , immunology , lymphocyte , interleukin 2 , cytotoxic t cell , biology , immune system , chemistry , t cell , in vitro , biochemistry , interleukin 21
Studies were made to determine whether freshly isolated monocytes from healthy donors could influence the induction of lymphokine (IL‐2)‐activated killer (LAK) activity. Highly purified lymphocytes ( > 99%) and monocytes (>90%) were isolated by counter‐flaw centrifugal elutriation from peripheral blood. Lymphocytes incubated for 4 days with IL‐2 showed significant LAK activity against natural killer (NK) cell‐resistant target (Daudi) cells, whereas monocytes treated for 4 days with IL‐2 and/or IFN‐γ were not cytotoxic. Under the experimental conditions used, addition of monocytes to the lymphocyte cultures resulted in significant augmentation of the LAK activity, depending on the density of monocytes added. In contrast, monocytes stimulated by lipopolysaccha‐ride (LPS) markedly suppressed LAK activity induced by IL‐2, depending on the dose of LPS added. Similar up‐ and down‐regulations of LAK cell induction by monocytes were observed with 4 lines of human lung cancer cells as targets for LAK activity. Although supernatants from untreated monocytes did not increase LAK induction, supernatants from LPS‐stimulated monocytes suppressed LAK induction. The regulatory role of monocytes could not be replaced by the addition of exogenous interleukin I (IL‐1) or tumor necrosis factor (TNF). Prostaglandin E did not seem to play a regulatory role, since addition of indomethacin did not affect the regulation of LAK cell induction by monocytes‐ These results clearly indicate that human monocytes may cause up‐ or down‐regulation of the expression of IL‐2 induced LAK activity, depending on their functional state.