The role of TNF‐α in Trichuris muris infection II: global enhancement of ongoing Th1 or Th2 responses

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Abstract
SUMMARY: Host resistance to Trichuris muris is driven by Th2 responses. However, TNF‐α has also been shown to play a role in protection. As TNF‐α has a variety of actions, the exact role of TNF‐α in immunity to T. muris is yet to be established. Here we demonstrate that although blocking TNF‐α has been shown to abrogate resistance, rTNF‐α treatment does not promote resistance. Further, we show that TNF‐α functions to enhance the ongoing immune response. AKR animals that typically respond to infection with a polarized Th1 response produce greater levels of Th1 cytokines when treated with TNF‐α and BALB/c animals that normally respond with a polarized Th2 response produce higher levels of Th2 cytokines. Crucially, blocking TNF‐α in the strong Th2 responder strain BALB/c does not prevent expulsion of T. muris, thus supporting its role as a biological enhancer. TNF‐α does increase transcription of both IFN‐γ and IL‐13 in vitro but can also act synergistically with IL‐13 in vitro to promote production of RELMβ, which has also been shown to play a role in resistance to T. muris. Thus, this data demonstrates that TNF‐α acts to enhance an ongoing immune response but is not necessary for a strong protective Th2 response.

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