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. 2013 Mar 11;210(3):433–443. doi: 10.1084/jem.20111229

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© 2013 Kotlarz et al.

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Figure 4. — Clinical and immunological phenotype and identification of IL-21R deficiency in family B. (A) Pedigree of family B. (B) Chest computed tomography (CT) showing extensive bronchiectasis. P. aeruginosa was cultured from bronchoalveolar lavage after this CT. (C) Magnetic resonance imaging/magnetic resonance cholangiopancreatography of the liver showing extensive intra and extrahepatic biliary duct dilatation. (D) Modified acid fast staining of bronchoalveolar lavage showing abundant neutrophils and Cryptosporidium. (E) FACS analysis of STAT phosphorylation (p-STAT1 Y701, p-STAT3 Y705, and p-STAT5 Y694) in PBMCs isolated from healthy donors (HD), mother (B.I-1), and P3 upon stimulation with rh IL-21. Black line, HD, rh IL-21; dark gray line, B.I-1, rh IL-21; light gray shaded; P3, unstimulated; red line; P3, rh IL-21. (F) DNA Sanger sequencing revealed a homozygous deletion in the IL21R gene (c.240_245delCTGCCA, p.C81_H82del) in P3 and P4. In contrast, the parents showed a heterozygous genotype. (G) FACS analysis of B cell proliferation and class-switch in P3 and P4 upon stimulation with rh IL-21.