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. 2022 Nov 11;13:1035532. doi: 10.3389/fimmu.2022.1035532

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Copyright © 2022 Hanrath, Hatton, Gothe, Browne, Vowles, Leary, Cockell, Cowley, James, Hambleton and Duncan

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A model of IFNAR2 deficient human iPS-macrophages (IFNAR2 ^PT iPS-Mϕ). (A) Expression of pluripotency markers by IFNAR2 ^PT iPSC clones 6 and 11 by flow cytometry.(B) PCR showing clearance of Sendai virus vector from IFNAR2 ^PT iPSC clones 6 and 11. (C) Karyogram produced from SNP array showing no gross abnormalities in the previously unpublished IFNAR2 ^PT iPSC clone 6. Red bars indicate loss or single copy, grey indicates loss of heterozygosity on chromosome 21 in the region of IFNAR2 (representative of data in IFNAR2 ^PT clone 11). (D) Expression of macrophage surface markers in IFNAR2 ^PT (clone 6) and IFNAR2 ^WT (WT1) iPS-Mϕ by flow cytometry, representative of repeat experiments in IFNAR2 ^PT clone 11 and WT2. (E) Phagocytic uptake of Zymosan pHrodo particles in IFNAR2 ^PT (clone 6) and IFNAR2 ^WT (WT1) iPS-Mϕ, representative of repeat experiments in clone 11 and WT2. (F) Immunoblot of IFNAR2 and GAPDH in IFNAR2 ^WT (WT2) and IFNAR2 ^PT (clone 11) iPS-Mϕ, representative of repeat experiments in WT1 and clone 6. (G) Immunoblot of IFN-I signalling in IFNα2b (1000 IU/mL) treated IFNAR2 ^PT (clone 11) and IFNAR2 ^WT (WT1) iPS-Mϕ, representative of n = 3 independent experiments.