Selective loss of function variants in <i>IL6ST</i> cause Hyper-IgE syndrome with distinct impairments of T-cell phenotype and function.

Finally, overexpression of GP130 P498L in HEK293- IL6ST KO cells mirrored the defects observed in patient fibroblasts with significant reductions upon stimulation with IL-6, IL-11, IL-27 and LIF, while STAT3 phosphorylation in response to OSM was reduced but did not reach statistical significance ( P =0.0625) ( Figure 4A-E ).

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