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Related Experiment Video

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Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
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Immunomodulation by mucosal gene transfer using TGF-beta DNA

N A Kuklin1, M Daheshia, S Chun

  • 1Department of Microbiology, The University of Tennessee, Knoxville, Tennessee 37996-0845, USA.

The Journal of Clinical Investigation
|July 17, 1998
PubMed
Summary
This summary is machine-generated.

Mucosal gene transfer of transforming growth factor-beta (TGF-beta) DNA suppressed T cell immunity to herpes simplex virus (HSV) infection. While this enhanced susceptibility to systemic HSV, it reduced ocular lesion severity when administered prophylactically.

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Area of Science:

  • Immunology
  • Gene Therapy
  • Virology

Background:

  • Herpes simplex virus (HSV) infection triggers significant immunoinflammatory responses.
  • Modulating these responses is crucial for managing HSV-related pathology.
  • Cytokine-based gene therapy offers a potential strategy for immune modulation.

Purpose of the Study:

  • To evaluate the efficacy of mucosal DNA delivery of transforming growth factor-beta (TGF-beta) for immune suppression and modulation in HSV infection.
  • To assess the impact of TGF-beta gene transfer on T cell-mediated immunity and inflammatory responses to HSV.
  • To determine the therapeutic potential of mucosal TGF-beta DNA administration for controlling HSV-induced lesions.

Main Methods:

  • Intranasal administration of an eukaryotic expression vector encoding TGF-beta1 in an animal model.
  • Assessment of TGF-beta expression in lung and lymphoid tissues.
  • Measurement of T cell-mediated immune responses, including delayed-type hypersensitivity (DTH) reactions.
  • Evaluation of susceptibility to systemic HSV infection.
  • Analysis of ocular lesion severity following prophylactic and therapeutic mucosal TGF-beta DNA administration.

Main Results:

  • Single intranasal TGF-beta1 DNA administration resulted in gene expression in the lung and lymphoid tissues.
  • Suppressed T cell-mediated immune responses to HSV, with effects lasting at least 7 weeks (measured by DTH).
  • Treated animals exhibited increased susceptibility to systemic HSV infection.
  • Multiple prophylactic mucosal TGF-beta DNA administrations reduced the severity of ocular lesions.
  • Therapeutic treatment with TGF-beta DNA showed no significant effect on the immunoinflammatory response in ocular lesions.

Conclusions:

  • Direct mucosal gene transfer of immunomodulatory cytokines, such as TGF-beta, is a feasible method for modulating immunity.
  • This approach can influence the expression of inflammatory disorders, including those associated with HSV infection.
  • TGF-beta gene therapy presents a potential strategy for managing specific aspects of HSV pathology, particularly prophylactic control of ocular lesions, despite risks of systemic susceptibility.