Murine IL-10 gene transfer inhibits established collagen-induced arthritis and reduces adenovirus-mediated inflammatory responses in mouse liver

J Immunol. 2001 May 15;166(10):5970-8. doi: 10.4049/jimmunol.166.10.5970.

Abstract

The effects of homologous IL-10 administration during an established autoimmune disease are controversial, given its reported immunostimulatory and immunosuppressive properties. Studies of collagen-induced arthritis have shown efficacy with repeated administrations of IL-10; however, when the EBV IL-10 homologue was administered via adenovirus gene transfer technology the results were equivocal. Therefore, the present study was undertaken to elucidate the effects of prolonged homologous IL-10 administration via adenovirus-mediated gene delivery on the progression of established arthritis. Collagen type II (CII)-immunized mice received i.v. injections of 10(7) or 10(8) PFU of an E1-deleted adenoviral vector containing the murine IL-10 gene (AdIL-10), after arthritis onset. Mice were monitored for 3 wk for disease progression, and gene transduction was assessed by quantification of serum mIL-10. CII-specific cell-mediated and humoral immune responses were analyzed by lymph node cell proliferation, cytokine production, and anti-CII Ab responses. Furthermore, because adenoviral vectors have been reported to induce organ dysfunction due to cell-mediated immune responses to the viral Ags, we have also evaluated delayed-type hypersensitivity responses and reactive hepatitis to the systemically delivered adenovirus and whether the IL-10 produced could influence those responses. Sustained suppression of autoimmune arthritis and elevated serum levels of IL-10 were achieved in our study. AdIL-10 treatment reduced cell-mediated immune reactivity, but did not affect humoral responses. Furthermore, IL-10 was able to reduce, but not totally abrogate, adenovirus-induced hepatic inflammation. These findings provide further insights into the diverse interplay of immune processes involved in autoimmune inflammation and the mechanism of cytokine immunotherapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviruses, Human / genetics*
  • Adenoviruses, Human / immunology
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage*
  • Arthritis, Experimental / genetics
  • Arthritis, Experimental / immunology
  • Arthritis, Experimental / prevention & control*
  • Collagen* / antagonists & inhibitors
  • Epitopes, T-Lymphocyte / immunology
  • Genetic Vectors / administration & dosage
  • Genetic Vectors / immunology
  • Hindlimb
  • Humans
  • Hypersensitivity, Delayed / immunology
  • Hypersensitivity, Delayed / pathology
  • Hypersensitivity, Delayed / virology
  • Immunoglobulin G / biosynthesis
  • Immunoglobulin G / blood
  • Immunosuppressive Agents / administration & dosage*
  • Injections, Intraperitoneal
  • Injections, Intravenous
  • Injections, Subcutaneous
  • Interleukin-10 / administration & dosage
  • Interleukin-10 / genetics*
  • Liver / immunology
  • Liver / pathology*
  • Liver / virology
  • Lymphocyte Activation / genetics
  • Male
  • Mice
  • Mice, Inbred DBA
  • T-Lymphocytes / immunology
  • Transduction, Genetic*

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Epitopes, T-Lymphocyte
  • Immunoglobulin G
  • Immunosuppressive Agents
  • Interleukin-10
  • Collagen