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Adenovirus early region 3 antiapoptotic 10.4K, 14.5K, and 14.7K genes decrease the incidence of autoimmune diabetes in NOD mice. | LitMetric

AI Article Synopsis

  • - The early region 3 (E3) genes of adenovirus help the virus dodge the host's immune system by disrupting critical processes like antigen presentation and programmed cell death (apoptosis).
  • - In a study using NOD mice with a specific genetic modification (RIPE3/NOD), it was found that the complete expression of E3 genes offered strong protection against autoimmune type 1 diabetes (T1D) by keeping beta cells safe from immune attacks.
  • - Mice lacking the gp19K gene showed significant T1D protection by suppressing immune markers, while those expressing gp19K but missing other E3 genes had weaker protection, indicating that all E3 genes need to work together to effectively prevent diabetes

Article Abstract

Genes in the early region 3 (E3) of the adenovirus genome allow the virus to evade host immune responses by interfering with major histocompatibility (MHC) class I-mediated antigen presentation and tumor necrosis factor-alpha (TNF-alpha)- or Fas-induced apoptosis of infected cells. Autoimmune type 1 diabetes (T1D) is inhibited in NOD mice transgenically expressing all E3 genes under control of a rat insulin promoter (RIPE3/NOD). For dissecting the protective mechanisms afforded by various E3 genes, they were subdivided into RIP-driven transgene constructs. Strong T1D protection mediated at the beta-cell level characterized DL704/NOD mice lacking the E3 gp19K gene suppressing MHC class I expression but retaining the 10.4K, 14.5K, and 14.7K genes inhibiting Fas- or TNF-alpha-induced apoptosis and TNF-alpha-induced NF-kB activation. Much weaker protection characterized DL309/NOD mice expressing the gp19K but not the 10.4K, 14.5K, and 14.7K genes. While RIPE3/NOD splenocytes had an unexpected decrease in ability to adoptively transfer T1D, splenocytes from both the DL704 and DL309 stocks efficiently did so. These findings indicate that all E3 genes must be expressed to inhibit the diabetogenic potential of NOD immune cells. They also demonstrate that the antiapoptotic E3 genes most effectively protect pancreatic beta-cells from diabetogenic immune responses.

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Source
http://dx.doi.org/10.2337/diabetes.52.5.1119DOI Listing

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