The authors began their study by examining IL-4-induced signalling in the reactive lymph nodes of mice infected with the TH2 cell-inducing enteric helminth Heligmosomoides polygyrus. Previous study of helminth infections had suggested that IL-4-induced signalling may be highly restricted to follicular lymphocyte populations. However, following infection with H. polygyrus, phosphorylated signal transducer and activator of transcription 6 (STAT6) could be detected in almost all B and T cells throughout the draining mesenteric lymph nodes. No STAT6 phosphorylation was observed in lymphocytes from infected IL-4-deficient or IL-4 receptor-α-deficient mice, indicating that lymphocyte expression of phosphorylated STAT6 was a specific indicator of IL-4-induced activation.
To determine whether similar widespread IFNγ signalling also occurred during a TH1-type response, the authors infected mice orally with the TH1 cell-inducing intracellular parasite Toxoplasma gondii and examined phosphorylation of STAT1. Most lymphocytes from the draining lymph nodes of T. gondii-infected mice contained phosphorylated STAT1 and surface-bound IFNγ — indicating that IFNγ, like IL-4, can signal throughout the entire lymph node. By contrast, the actions of the TH1 cell-polarizing cytokine IL-12 were found to be tightly restricted following T. gondii infection, with only a small number of T cells in the draining lymph nodes showing evidence of IL-12-induced signalling.
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