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CORRECTION article

Front. Immunol., 10 May 2023
Sec. Primary Immunodeficiencies
Volume 14 - 2023 | https://doi.org/10.3389/fimmu.2023.1212029

Corrigendum: Vulnerability to meningococcal disease in immunodeficiency due to a novel pathogenic missense variant in NFKB1

This article is a correction to:

  1. Vulnerability to Meningococcal Disease in Immunodeficiency Due to a Novel Pathogenic Missense Variant in NFKB1

    1. Read original article
Manfred Anim,Manfred Anim1,2Georgios Sogkas,Georgios Sogkas1,3Gunnar SchmidtGunnar Schmidt4Natalia DubrowinskajaNatalia Dubrowinskaja1Torsten WitteTorsten Witte1Reinhold Ernst Schmidt,Reinhold Ernst Schmidt1,3Faranaz Atschekzei,*Faranaz Atschekzei1,3*
  • 1Department of Rheumatology and Immunology, Hannover Medical School, Hannover, Germany
  • 2Hannover Biomedical Research School (HBRS), Hannover Medical School, Hanover, Germany
  • 3RESIST - Cluster of Excellence 2155 to Hanover Medical School, Satellite Center Freiburg, Hanover, Germany
  • 4Department of Human Genetics, Hannover Medical School, Hannover, Germany

A Corrigendum on
Vulnerability to meningococcal disease in immunodeficiency due to a novel pathogenic missense variant in NFKB1.

by Anim M, Sogkas G, Schmidt G, Dubrowinskaja N, Witte T, Schmidt RE and Atschekzei F (2021) Front. Immunol. 12:767188. doi: 10.3389/fimmu.2021.767188

In the published article, there was an error in Figure 1 as published. We recognized that the loading control (β-actin) in Figure 1E is identical with 1D and has to be replaced with the correct loading control.

FIGURE 1
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Figure 1 Monoallelic NFKB1 missense mutation in a family with late-onset antibody deficiency. (A) Segregation of NFKB1variant was analyzed by sequencing genomic PCR product and revealed an autosomal-dominant inheritance in families with reduced clinical penetrance. The analysis excluded the mother of patients because of material lack. (B) Sanger sequencing of genomic PCR products results in the chromatogram of missense variant and wild type (WT) (C) Structure of NFκB protein showing the position of the identified mutation. (D) Immunoblotting was performed in PBMCs of subjects (S1, S2, and S3) and healthy control (HC), and the expression of p105/50 was evaluated. The expression of p105 was reduced for all the subjects compared to the control. However, the expression of p50 was reduced in S2. (E) PBMCs from HC and S1, S2 and S3 were stimulated with PMA; 50 ng/ml and ionomycin; 1 μg/ml and the expression of p105/50 evaluated. There were no significant changes in the p105/50 expression after stimulation in the subjects; however, p105 phosphorylation at serine 933 was detected in only the HC but not in the subject. Beta-actin was used as a cytoplasmic loading control.

The corrected Figure 1 and its caption [Monoallelic NFKB1 missense mutation in a family with late-onset antibody deficiency. (A) Segregation of NFKB1variant was analyzed by sequencing genomic PCR product and revealed an autosomal-dominant inheritance in families with reduced clinical penetrance. The analysis excluded the mother of patients because of material lack. (B) Sanger sequencing of genomic PCR products results in the chromatogram of missense variant and wild type (WT) (C) Structure of NFκB protein showing the position of the identified mutation. (D) Immunoblotting was performed in PBMCs of subjects (S1, S2, and S3) and healthy control (HC), and the expression of p105/50 was evaluated. The expression of p105 was reduced for all the subjects compared to the control. However, the expression of p50 was reduced in S2. (E) PBMCs from HC and S1, S2 and S3 were stimulated with PMA; 50 ng/ml and ionomycin; 1 μg/ml and the expression of p105/50 evaluated. There were no significant changes in the p105/50 expression after stimulation in the subjects; however, p105 phosphorylation at serine 933 was detected in only the HC but not in the subject. Beta-actin was used as a cytoplasmic loading control.] appear below.

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Keywords: common variable immune deficiency (CVID), NFKB1, Nfkb1 (p50), hypogammaglobulinemia, primary antibody deficiency (PAD)

Citation: Anim M, Sogkas G, Schmidt G, Dubrowinskaja N, Witte T, Schmidt RE and Atschekzei F (2023) Corrigendum: Vulnerability to meningococcal disease in immunodeficiency due to a novel pathogenic missense variant in NFKB1. Front. Immunol. 14:1212029. doi: 10.3389/fimmu.2023.1212029

Received: 25 April 2023; Accepted: 27 April 2023;
Published: 10 May 2023.

Edited and Reviewed by:

Anders Fasth, University of Gothenburg, Sweden

Copyright © 2023 Anim, Sogkas, Schmidt, Dubrowinskaja, Witte, Schmidt and Atschekzei. 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.

*Correspondence: Faranaz Atschekzei, Atschekzei.Faranaz@mh-hannover.de

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.