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Specific antibody deficiency and autoinflammatory disease extend the clinical and immunological spectrum of heterozygous NFKB1 loss-of-function mutations in humans

2016; Ferrata Storti Foundation; Volume: 101; Issue: 10 Linguagem: Inglês

10.3324/haematol.2016.145136

1592-8721

Cyrill Schipp, Schafiq Nabhani, K. Bienemann, Natalia Simanovsky, Shlomit Kfir-erenfeld, Nathalie Assayag-Asherie, Prasad T. Oommen, Shoshana Revel‐Vilk, Andrea Hönscheid, Michael Gombert, Sebastian Ginzel, Daniel W. Schafer, Hans-Juergen Laws, Eitan Yefenof, Bernhard Fleckenstein, Arndt Borkhardt, Polina Stepensky, Ute Fischer,

Cytokine Signaling Pathways and Interactions

The nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (NF-κB1) is a master regulator of immune and inflammatory responses.[1][1],[2][2] NF-κB1 belongs to the NF-κB/Rel family of transcription factors that consists of five members in humans: NF-κB1 (p105/p50), NF-κB2 (p100/p52