Deficient interleukin‐2 responsiveness of T lymphocytes from patients with primary biliary cirrhosis

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 inv...

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Bibliographic Details
Published in:Hepatology (Baltimore, Md.) Md.), 1992-10, Vol.16 (4), p.931-936
Main Authors: Menéndez, José Luis, Girón, José Antonio, Manzano, Luis, Garrido, Aurelio, Abreu, Luis, Albillos, Agustin, Durántez, Alberto, Alvarez‐Mon, Melchor
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cell Division - drug effects
Gastroenterology. Liver. Pancreas. Abdomen
Humans
Interleukin-2 - biosynthesis
Interleukin-2 - pharmacology
Liver Cirrhosis, Biliary - pathology
Liver Cirrhosis, Biliary - physiopathology
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Lymphocyte Activation
Medical sciences
Middle Aged
Other diseases. Semiology
Phytohemagglutinins - pharmacology
T-Lymphocytes - drug effects
T-Lymphocytes - metabolism
T-Lymphocytes - physiology
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Summary: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.)
ISSN:0270-9139
1527-3350
DOI:10.1002/hep.1840160413