TNFα DNA vaccination prevents clinical manifestations of experimental antiphospholipid syndrome

M. Blank, I. Krause, G. Wildbaum, N. Karin, Y. Shoenfeld

Research output: Contribution to journalArticlepeer-review

Abstract

Naked DNA encoding TNFα was introduced to BALB/c mice with experimental antiphospholipid syndrome (APS) induced by β2GPI. Administration of naked DNA encoding TNFα resulted in the generation of immunological memory to its gene product, associated with elevated circulating anti-TNFα antibodies. Enriched IgG fraction of the mouse anti-TNFα was biologically active since it prevented endothelial cell activation by TNFα, e.g., inhibition of monocyte adhesion to activated endothelial cells (HUVEC). Mice immunized with β2GPI, vaccinated with TNFα DNA at an early stage of disease development, showed decreased titres of circulating anti-β2GPI antibodies as compared to the group of mice vaccinated with a control naked DNA. The reduction of antiphospholipid antibody production was followed by amelioration of the foetal loss, increased platelet count to normal values as well as normalization of the prolonged aPTT. APS mice which were introduced to the TNFα DNA vector at a later stage of the disease development, showed less improvement in their clinical manifestations. The current study suggests a way in which a DNA vaccine can be employed for induction of a protective immunity in experimental APS.

Original languageEnglish
Pages (from-to)546-549
Number of pages4
JournalLupus
Volume12
Issue number7
DOIs
StatePublished - 2003
Externally publishedYes

Keywords

  • Anti-β2glycoprotein I autoimmunity
  • Antiphospholipid syndrome
  • DNA vaccination
  • Tumor necrosis factor

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