Transduction of a foreign histocompatibility gene into the arterial wall induces vasculitis

Elizabeth G. Nabel, Gregory Plautz, Gary J. Nabel

Research output: Contribution to journalArticle

Abstract

Autoimmune vasculitis represents a disease characterized by focal inflammation within arteries at multiple sites in the vasculature. Therapeutic interventions in this disease are empirical and often unsuccessful, and the mechanisms of immune injury are not well-defined. The direct transfer of recombinant genes and their expression in the arterial wall provides an opportunity to explore the pathogenesis and treatment of vascular disease. In this report, an animal model for vasculitis has been developed. Inflammation has been elicited by direct gene transfer of a foreign class I major histocompatibility complex gene, HLA-B7, to specific sites in porcine arteries. Transfer and expression of this recombinant gene was confirmed by a polymerase chain reaction and immunohistochemistry, and cytolytic T cells specific for HLA-B7 were detected. These findings demonstrate that expression of a recombinant gene in the vessel wall can induce a focal immune response and suggest that vessel damage induced by cell-mediated immune injury can initiate vasculitis. (.

Original languageEnglish (US)
Pages (from-to)5157-5161
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume89
Issue number11
StatePublished - 1992
Externally publishedYes

Fingerprint

Histocompatibility
Vasculitis
HLA-B7 Antigen
Arteries
Genes
Inflammation
Gene Expression
Wounds and Injuries
Major Histocompatibility Complex
Vascular Diseases
Swine
Animal Models
Immunohistochemistry
T-Lymphocytes
Polymerase Chain Reaction
Therapeutics

Keywords

  • Gene therapy
  • Liposomes
  • Retroviral vector

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Transduction of a foreign histocompatibility gene into the arterial wall induces vasculitis. / Nabel, Elizabeth G.; Plautz, Gregory; Nabel, Gary J.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 89, No. 11, 1992, p. 5157-5161.

Research output: Contribution to journalArticle

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