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Deficient interleukin‐2 responsiveness of T lymphocytes from patients with primary biliary cirrhosis
Author(s) -
Menéndez José Luis,
Girón José Antonio,
Manzano Luis,
Garrido Aurelio,
Abreu Luis,
Albillos Agustin,
Durántez Alberto,
AlvarezMon Melchor
Publication year - 1992
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840160413
Subject(s) - primary biliary cirrhosis , ionomycin , medicine , interleukin 2 , endocrinology , ursodeoxycholic acid , hepatology , immune system , biliary cirrhosis , interleukin , cirrhosis , immunology , receptor , cytokine , biology , stimulation , autoimmune disease , disease
There is increasing evidence that primary biliary cirrhosis is associated with an alteration of the immune system. Although the cause remains unknown, it has been suggested that the immune system of patients with primary biliary cirrhosis is involved in the pathogenesis of their disease. We have investigated the T‐cell function in patients with primary biliary cirrhosis and have found defective phytohemagglutinin‐induced T‐cell mitogenesis. Likewise, their blastogenic response to CD3 monoclonal antibody was also depressed, although the DNA synthesis induced by stimulation with phorbol esters (12‐O‐tetradecanoilphorbol‐13‐acetate) plus ionophore (ionomycin) was normal. These alterations could not be ascribed either to a decreased synthesis of interleukin‐2 or to a defective expression of interleukin‐2 receptor after cellular activation. Moreover, this defective proliferative response of T lymphocytes was observed even in the presence of saturating concentrations of exogenous interleukin‐2. These results represent evidence of the deficiency in the interleukin‐2—dependent pathway found in T lymphocytes from patients with primary biliary cirrhosis. (HEPATOLOGY 1992;16:931–936.)