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Regulation of Natural Killer Cell Activity by Transforming Growth Factor‐β and Prostaglandin E 2
Author(s) -
MALYGIN A. M.,
MERI S.,
TIMONEN T.
Publication year - 1993
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.1365-3083.1993.tb01667.x
Subject(s) - transforming growth factor , prostaglandin , natural killer cell , prostaglandin e , microbiology and biotechnology , immunology , biology , endocrinology , biochemistry , cytotoxicity , in vitro
The separate and combined effects of transforming growth factor‐β1 (TGF‐β1) and prostaglandin E 2 on human natural killer (NK) activity were studied. Peripheral blood lymphocytes (PBL) and large granular lymphocytes (LGL, 70–90% purity) were used as effector cells and K562 as targets. Overnight incubation of the effector cells with TGF‐β1 resulted in a significant inhibition of NK activity. TGF‐β1 did not influence the expression of CD3, CD 16, CD 18 or CD56 antigens on PBL. Combination of TGF‐βl with indomethacin gave the same NK‐suppressive effect as TGE‐β1 alone, showing that the inhibition of NK acuvity by TGF‐β1 is not due to an increase in PGE 2 levels. TGF‐β did not influence cAMP level in PBL whereas PGE 2 significantly increased it. On the other hand. TGE‐β1 and PGE 2 showed an additive inhibitory effect on NK activity. TGF‐β1 did not reduce the binding of PBL and LGL to K562. PGE 2 suppressed the binding and TGF‐β1 did not influence this suppression. TGF‐β1 also suppressed IL‐2‐induced activation of NK activity and increase of expression of the granule proteins granzyme A and perforin. PGE 2 did not appear to affect granzyme A and perforin contents. The results indicate that TGF‐β1 and PGE 2 suppress NK activity by different mechanisms.