Article Text

Download PDFPDF
Original article
IL-26 is overexpressed in chronically HCV-infected patients and enhances TRAIL-mediated cytotoxicity and interferon production by human NK cells
  1. Charline Miot1,2,3,11,
  2. Elodie Beaumont4,5,
  3. Dorothée Duluc1,2,3,
  4. Hélène Le Guillou-Guillemette6,7,
  5. Laurence Preisser1,2,3,
  6. Erwan Garo1,2,3,
  7. Simon Blanchard1,2,3,11,
  8. Isabelle Hubert Fouchard8,
  9. Christophe Créminon9,
  10. Patricia Lamourette9,
  11. Isabelle Fremaux1,2,3,
  12. Paul Calès7,8,
  13. Françoise Lunel-Fabiani6,7,
  14. Jérôme Boursier8,
  15. Oliver Braum10,
  16. Helmut Fickenscher10,
  17. Philippe Roingeard4,5,
  18. Yves Delneste1,2,3,11,
  19. Pascale Jeannin1,2,3,11
  1. 1Université d'Angers, Angers, France
  2. 2Inserm, Unité 892, Angers, France
  3. 3CNRS, Unité 6299, Angers, France
  4. 4Université de Tours, Tours, France
  5. 5Inserm, Unité 966, Tours, France
  6. 6Laboratoire de Bactériologie-Virologie, CHU Angers, Angers, France
  7. 7Université d'Angers, UPRES 3859, Angers, France
  8. 8Service d'Hépato-Gastroentérologie, CHU Angers, Angers, France
  9. 9Service de Pharmacologie et d'Immunoanalyse, Commissariat à l'Energie Atomique Saclay, iBiTec-S, Gif sur Yvette, France
  10. 10Institute for Infection Medicine, Christian Albrecht University of Kiel and University Medical Center Schleswig-Holstein, Kiel, Germany
  11. 11Laboratoire d'Immunologie et Allergologie, CHU Angers, Angers, France
  1. Correspondence to Professor Pascale Jeannin, Unité Inserm 892—CNRS 6299, Institut de biologie en santé (PBH-IRIS), CHU d'Angers, 4 rue Larrey, 49933 Angers, France; pascale.jeannin{at}


Objective Interleukin-26 (IL-26) is a member of the IL-10 cytokine family, first discovered based on its peculiar expression by virus-transformed T cells. IL-26 is overexpressed in chronic inflammation (rheumatoid arthritis and Crohn’s disease) and induces proinflammatory cytokines by myeloid cells and some epithelial cells. We thus investigated the expression and potential role of IL-26 in chronic HCV infection, a pathology associated with chronic inflammation.

Design IL-26 was quantified in a cohort of chronically HCV-infected patients, naive of treatment and its expression in the liver biopsies investigated by immunohistochemistry. We also analysed the ability of IL-26 to modulate the activity of natural killer (NK) cells, which control HCV infection.

Results The serum levels of IL-26 are enhanced in chronically HCV-infected patients, mainly in those with severe liver inflammation. Immunohistochemistry reveals an intense IL-26 staining in liver lesions, mainly in infiltrating CD3+ cells. We also show that NK cells from healthy subjects and from HCV-infected patients are sensitive to IL-26. IL-26 upregulates membrane tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) expression on CD16− CD56bright NK cells, enabling them to kill HCV-infected hepatoma cells, with the same efficacy as interferon (IFN)-α-treated NK cells. IL-26 also induces the expression of the antiviral cytokines IFN-β and IFN-γ, and of the proinflammatory cytokines IL-1β and TNF-α by NK cells.

Conclusions This study highlights IL-26 as a new player in the inflammatory and antiviral immune responses associated with chronic HCV infection.

  • HCV

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.