Medical Journals

Enhancement of Ifn-gamma Production for Th1-cell Therapy Using Negatively Charged Liposomes Containing Phosphatidylserine.

Authors:
  • Yotsumoto Satoshi
  • Kakiuchi Terutaka
  • Aramaki Yukihiko

From: Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.

Vaccine

  • Publish Date: Jul 2007
  • ISSN: 0264-410X
  • Volume: 25
  • Issue: 29
  • Pages: 5256-62
  • Medium: Print
  • Language: English
  • Citation (JAMA): Yotsumoto Satoshi, Kakiuchi Terutaka, Aramaki Yukihiko, et al. Enhancement of Ifn-gamma Production for Th1-cell Therapy Using Negatively Charged Liposomes Containing Phosphatidylserine.. Vaccine Jul 2007;25:5256-62

Abstract

We have developed an efficient method of interferon-gamma (IFN-gamma) induction for Th1-cell therapy. OVA (ovalbumin)-specific Th1 clone 42-6A cells cocultured with antigen presenting cells (APCs) from spleen resulted in high levels of OVA-specific IFN-gamma production by the treatment of phosphatidylserine (PS), but not phosphatidic acid (PA), liposomes-encapsulated OVA (OVA-liposomes). The IFN-gamma production was increased in a manner dependent on the PS content of the liposomes and inhibited by the addition of annexin V, a PS binding protein. Furthermore, coadministration of Th1 cells plus OVA-liposomes in mice strikingly enhanced IFN-gamma levels in serum and in spleen cells compared with that of Th1 cells plus OVA. In addition, serum levels of IL-12 p70 increased and ongoing OVA-specific IgE immune response was dramatically attenuated. These results first suggest that antigen delivery using negatively charged liposomes containing PS is very useful for the enhancement of IFN-gamma production in Th1-cell therapy.

Mesh Headings (Keywords): Animals, Antigen-Presenting Cells, Cells, Cultured, Coculture Techniques, Immunoglobulin E, Immunologic Factors, Interferon Type II, Interleukin-12, Liposomes, Mice, Mice, Inbred BALB C, Models, Animal, Ovalbumin, Phosphatidylserines, Th1 Cells


Check for Full Text / PubMed Unique Identifier (PMID): 17583394


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


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