Inhibition of autoimmune type 1 diabetes by gastrointestinal helminth infection

K. Saunders, T. Raine, A. Cooke, C. Lawrence

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171 Citations (Scopus)


Gastrointestinal nematode infections are prevalent worldwide and are potent inducers of T helper 2 responses with the capacity to modulate the immune response to heterologous antigens. Parasitic helminth infection has even been shown to modulate the immune response associated with autoimmune diseases. Nonobese diabetic (NOD) mice provide a model for studying human autoimmune diabetes; as in humans, the development of diabetes in NOD mice has been linked to the loss of self-tolerance to beta cell autoantigens. Previous studies with the NOD mouse have shown that helminth and bacterial infection appears to inhibit type 1 diabetes by disrupting the pathways leading to the Th1-mediated destruction of insulin-producing beta cells. The aim of our study was to examine whether infection with the gastrointestinal helminths Trichinella spiralis or Heligmosomoides polygyrus could inhibit the development of autoimmune diabetes in NOD mice and to analyze the mechanisms involved in protection and the role of Th2 responses. Protection from diabetes was afforded by helminth infection, appeared to inhibit autoimmune diabetes by disrupting pathways leading to the destruction of beta cells, and was mediated by seemingly independent mechanisms depending on the parasite but which may be to be related to the capacity of the host to mount a Th2 response.
Original languageEnglish
Pages (from-to)397-407
Number of pages11
JournalInfection and Immunity
Issue number1
Early online date16 Oct 2006
Publication statusPublished - Jan 2007


  • gastrointestinal nematode infections
  • T helper 2 responses
  • immune response
  • heterologous antigens
  • parasitic helminth infection
  • autoimmune disease


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