A Proinflammatory Role For Interleukin-22 In The Immune Response To Hepatitis B Virus.

[Guest guest]

Gastroenterology. 2011 Jun 24. [Epub ahead of print]

A Proinflammatory Role For Interleukin-22 In The Immune Response To Hepatitis B

Virus.

Zhang Y, Cobleigh MA, Lian JQ, Huang CX, Booth CJ, Bai XF, Robek MD.

Source

Department of Pathology, Yale University School of Medicine, New Haven, CT,

06510, USA; Center for Infectious Diseases, Tangdu Hospital, Fourth Military

Medical University, Xi'an, Shaanxi Province, 710038, China.

Abstract

BACKGROUND & AIMS:

T-helper (Th)17 cells that secrete interleukin (IL)-22 have immunomodulatory and

protective properties in the liver and other tissues. IL-22 induces expression

of proinflammatory genes, but is also mitogenic and anti-apoptotic in

hepatocytes. Therefore, it could have multiple functions in the immune response

to hepatitis B virus (HBV).

METHODS:

We examined the role of IL-22 in regulating liver inflammation in HBV transgenic

mice and measured levels of IL-22 in HBV-infected patients.

RESULTS:

In HBV transgenic mice, injection of a single dose of IL-22 increased hepatic

expression of proinflammatory genes, but did not directly inhibit virus

replication. When splenocytes from HBV-immunized mice were transferred into HBV

transgenic mice, the severity of the subsequent liver damage was ameliorated by

neutralization of IL-22. In this model, IL-22 depletion did not affect

interferon-ã- mediated noncytopathic inhibition of virus replication initiated

by HBV-specific cytotoxic T cells, but it significantly inhibited recruitment of

antigen-non-specific inflammatory cells into the liver. In patients with acute

HBV infections, the percentage of Th17 cells in peripheral blood and

concentration of IL-22 in serum were significantly increased.

CONCLUSION:

IL-22 appears to be an important mediator of the inflammatory response following

recognition of HBV by T cells in the liver. These findings might be relevant to

the development of cytokine-based therapies for patients with HBV infection.

Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.

PMID: 21708106 [PubMed - as supplied by publisher]

[Guest guest]

Gastroenterology. 2011 Jun 24. [Epub ahead of print]

A Proinflammatory Role For Interleukin-22 In The Immune Response To Hepatitis B

Virus.

Zhang Y, Cobleigh MA, Lian JQ, Huang CX, Booth CJ, Bai XF, Robek MD.

Source

Department of Pathology, Yale University School of Medicine, New Haven, CT,

06510, USA; Center for Infectious Diseases, Tangdu Hospital, Fourth Military

Medical University, Xi'an, Shaanxi Province, 710038, China.

Abstract

BACKGROUND & AIMS:

T-helper (Th)17 cells that secrete interleukin (IL)-22 have immunomodulatory and

protective properties in the liver and other tissues. IL-22 induces expression

of proinflammatory genes, but is also mitogenic and anti-apoptotic in

hepatocytes. Therefore, it could have multiple functions in the immune response

to hepatitis B virus (HBV).

METHODS:

We examined the role of IL-22 in regulating liver inflammation in HBV transgenic

mice and measured levels of IL-22 in HBV-infected patients.

RESULTS:

In HBV transgenic mice, injection of a single dose of IL-22 increased hepatic

expression of proinflammatory genes, but did not directly inhibit virus

replication. When splenocytes from HBV-immunized mice were transferred into HBV

transgenic mice, the severity of the subsequent liver damage was ameliorated by

neutralization of IL-22. In this model, IL-22 depletion did not affect

interferon-ã- mediated noncytopathic inhibition of virus replication initiated

by HBV-specific cytotoxic T cells, but it significantly inhibited recruitment of

antigen-non-specific inflammatory cells into the liver. In patients with acute

HBV infections, the percentage of Th17 cells in peripheral blood and

concentration of IL-22 in serum were significantly increased.

CONCLUSION:

IL-22 appears to be an important mediator of the inflammatory response following

recognition of HBV by T cells in the liver. These findings might be relevant to

the development of cytokine-based therapies for patients with HBV infection.

Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.

PMID: 21708106 [PubMed - as supplied by publisher]