IL-12R deficiency and Job's (Hyper IgE)

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Transformers

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Pathwise...both are decreased Th1 response and decreased IFN-y production...IL12R leads to probs with essentially forming granulmoas to wall off Tb since your macrophages arent activated..

In HyperIgE (Jobs syndrome) I dont get the relationship between Th1 cells failing to produce IFN-y (when did IFN-y ever become a chemotactic factor???) and the inability for neutrophils to respond to chemotactic stimuli OTHER than some pathway that since your macrophages aren't activated and hence don't make IL-8 to chemoattract neutrophils

which makes me think HyperIgE is a more downstream path of IL-12R..Im overthinking this

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