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(American Journal of Pathology. 2000;157:1685-1692.)
© 2000 American Society for Investigative Pathology

Regular Articles

Defective Interleukin-1 Receptor Antagonist Production Is Associated with Resistance of Acute Liver Graft Rejection to Steroid Therapy

Filomena Conti*{dagger}, Sylvie Breton*, Frédéric Batteux{dagger}, Valérie Furlan{ddagger}, Didier Houssin§, Bernard Weill{dagger} and Yvon Calmus*{dagger}

From the Laboratoire de Biologie Cellulaire*
and the Laboratoire d’Immunologie,{dagger}
Faculté de Médecine Cochin-Port-Royal, Université Paris; the Pharmacie,{ddagger}
Hôpital Bicêtre; and the Service de Chirurgie Générale et de Transplantation Hépatique,§
Hôpital Cochin, Paris, France

Thirty percent of acute liver graft rejection episodes are resistant to steroids. As interleukin-1 (IL-1) is an important target of steroid therapy, we examined the possible involvement of reduced sensitivity of IL-1 production to steroids or defective production of its antagonist, IL-1Ra. Patients were assessed during steroid-sensitive or -resistant rejection and 2 years later. In situ IL-1ß and IL-1Ra expression was evaluated by immunohistochemistry; their production was assayed by enzyme-linked immunosorbent assay and the gene polymorphisms by reverse transcriptase-polymerase chain reaction on blood cells. Hepatic IL-1ß and IL-1Ra expression were enhanced during rejection. IL-1 production and its inhibition by steroids were similar in steroid-responsive and steroid-resistant rejection. However, IL-1Ra production was lower in steroid-resistant than in steroid-responsive rejection, and this difference was still observed 2 years after rejection. IL-1ß and IL-1Ra gene polymorphisms did not differ between patients with and without steroid resistance. Low IL-1Ra production is associated with steroid resistance of acute rejection and is due to a constitutional defect. The early identification of such patients might qualify them for stronger anti-rejection therapy, including IL-1Ra.




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