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. 2024 Jul 12;15:1402038. doi: 10.3389/fimmu.2024.1402038

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Copyright © 2024 Tahiat, Belbouab, Yagoubi, Hakem, Fernini, Keddari, Belhadj, Touri, Aggoune, Stoddard, Niemela, Zerifi, Melzi, Aboura, Saad-Djaballah, Ferhani, Ketfi, Messaoudi, Bencharif Madani, Benhacine, Dehimi, Okka, Amroune, Fellahi, Bendahmane, Khoulani, Oukil, Soufane, Bourelaf, Boubidi, Boukhenfouf, Amine Ifri, Khelafi, Boudiaf, Khelifi Touhami, Meçabih, Boucelma, Zelaci, Gacem, Ladj, Mekki, Bensaadi, Benhalima, Zeroual, Bioud, Benameur, Bouhdjila, Bouzerar, Ibsaine, Maouche, Kedji, Smati, Boukari, Lambert, Rosenzweig, Notarangelo and Djenouhat

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(A) Dot plots and histograms showing reduced IL-17A production (upper left panel), CD45RO⁺CCR6⁺CXCR3^– Th17 cells (upper middle panel), and pSTAT3 levels after IL-6 stimulation (upper right panel) in a patient with HIES. (B) Degranulation assay of resting NK cells showing impaired CD107a surface expression in a patient with FHL3. (C) Histograms showing partial perforin expression defect on gated CD3^–CD56⁺ NK cells in a patient with FHL2. FHL, familial hemophagocytic lymphohistiocytosis; HIES, hyper-IgE syndrome; IC, isotypic control; pSTAT3, phosphorylated signal transducer and activator of transcription 3.