TH9 immunodeficiency in patients with hyper-IgE syndrome

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TH9 immunodeficiency in patients with hyper-IgE syndrome Matthew R. Olson, PhD, Mark H. Kaplan, PhD  Journal of Allergy and Clinical Immunology  Volume 143, Issue 3, Pages 935-936 (March 2019) DOI: 10.1016/j.jaci.2018.10.044 Copyright © 2018 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Effect of STAT3 in TH9 development. In developing human TH9 cells (left), activation of STAT3 induces SOCS3, which represses the inhibitory STAT1 pathway activation but does not seem to affect the IL-9–promoting effects of STAT5. In patients with HIES with STAT3 LOF mutations, control of the inhibitory pathway is lost. In contrast, in developing mouse TH9 cells (right), STAT3 activation inhibits STAT5 activation that is required for maximal IL-9 production. Mouse STAT3 activation can also interfere with STAT1 activation, although the inhibitory effects of STAT1 in mouse cells is less defined, and the loss of STAT5 activation is the dominant effect. BCL6, B-cell lymphoma 6; SOCS3, suppressor of cytokine signaling 3. Journal of Allergy and Clinical Immunology 2019 143, 935-936DOI: (10.1016/j.jaci.2018.10.044) Copyright © 2018 American Academy of Allergy, Asthma & Immunology Terms and Conditions