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Immune Dysfunction in Primary Biliary Cirrhosis
Author(s) -
CHIRICOLO M,
LENZI M.,
BIANCHI F.,
FRANCESCHI C.,
BARTOLINI G.,
ORLANDI M.,
TOMASI V.,
LICASTRO F.
Publication year - 1989
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.1365-3083.1989.tb01222.x
Subject(s) - phytohaemagglutinin , peripheral blood mononuclear cell , primary biliary cirrhosis , medicine , monocyte , immunology , thromboxane b2 , thromboxane , endocrinology , immune system , population , lymphocyte , cirrhosis , in vitro , chemistry , platelet , biochemistry , environmental health
In a previous study we observed that after in vitro treatment with indomethacin, lymphocyte response to phytohaemagglutinin (PHA) in primary biliar) cirrhosis (PBC) patients was higher than that of controls. We know that indomethacin also inhibits prostanoid production, and thus in the present work we directly measured prostaglandin E 2 (PGE 2 ) and thromboxane B 2 (TXB 2 ) production by mononuclear cells and monocytes from 12PBC patients. 11 control subjects, and three control disease patients (alcoholic cirrhosis. AC). PHA‐stimulated enriched monocytes from PBC patients produced approximately threefold more PGE 2 (after 48 h of culture) than did normal and AC monocytes ( P <0.05). TXB 2 production was similar in all groups studied. We also made cultures in which PBC‐purified lymphocytes proliferated better than PBC mononuclear cells (i.e. lymphocytes plus monocytes). Thus, a monocyte population producing PGE 2 could be responsible, at least in part, for the hyporesponsiveness to PHA observed in PBC patients.