J 2023

Autoantibodies against type I IFNs in humans with alternative NF-.B pathway deficiency

TOM, Le Voyer, Audrey V PARENT, Xian LIU, Axel CEDERHOLM, Adrian GERVAIS et. al.

Basic information

Original name

Autoantibodies against type I IFNs in humans with alternative NF-.B pathway deficiency

Authors

TOM, Le Voyer, Audrey V PARENT, Xian LIU, Axel CEDERHOLM, Adrian GERVAIS, Jeremie ROSAIN, Tina NGUYEN, Malena Perez LORENZO, Elze RACKAITYTE, Darawan RINCHAI, Peng ZHANG, Lucy BIZIEN, Gonca HANCIOGLU, Pascale GHILLANI-DALBIN, Jean-Luc CHARUEL, Quentin PHILIPPOT, Mame Sokhna GUEYE, Majistor Raj Luxman Maglorius RENKILARAJ, Masato OGISHI, Camille SOUDEE, Melanie MIGAUD, Flore ROZENBERG, Mana MOMENILANDI, Quentin RILLER, Luisa IMBERTI, Ottavia M DELMONTE, Gabriele MUELLER, Baerbel KELLER, Julio ORREGO, William Alexander Franco GALLEGO, Tamar RUBIN, Melike EMIROGLU, Nima PARVANEH, Daniel ERIKSSON, Maribel ARANDA-GUILLEN, David I BERRIOS, Linda VONG, Constance H KATELARIS, Peter MUSTILLO, Johannes RAEDLER, Jonathan BOHLEN, Jale Bengi CELIK, Camila ASTUDILLO, Sarah WINTER, Catriona MCLEAN, Aurelien GUFFROY, Joseph L DERISI, David YU, Corey MILLER, Yi FENG, Audrey GUICHARD, Vivien BEZIAT, Jacinta BUSTAMANTE, Qiang PAN-HAMMARSTROM, Yu ZHANG, Lindsey B ROSEN, Steve M HOLLAND, Marita BOSTICARDO, Heather KENNEY, Riccardo CASTAGNOLI, Charlotte A SLADE, Kaan BOZTUG, Nizar MAHLAOUI, Sylvain LATOUR, Roshini S ABRAHAM, Vassilios LOUGARIS, Fabian HAUCK, Anna SEDIVA, Faranaz ATSCHEKZEI, Georgios SOGKAS, M Cecilia POLI, Mary A SLATTER, Boaz PALTERER, Michael D KELLER, Alberto PINZON-CHARRY, Anna SULLIVAN, Luke DRONEY, Daniel SUAN, Melanie WONG, Alisa KANE, Hannah HU, Cindy MA, Hana GROMBIŘÍKOVÁ (203 Czech Republic, belonging to the institution), Peter CIZNAR, Ilan DALAL, Nathalie ALADJIDI, Miguel HIE, Estibaliz LAZARO, Jose FRANCO, Sevgi KELES, Marion MALPHETTES, Marlene PASQUET, Maria Elena MACCARI, Andrea MEINHARDT, Aydan IKINCIOGULLARI, Mohammad SHAHROOEI, Fatih CELMELI, Patrick FROSK, Christopher C GOODNOW, Paul E GRAY, Alexandre BELOT, Hye Sun KUEHN, Sergio D ROSENZWEIG, Makoto MIYARA, Francesco LICCIARDI, Amelie SERVETTAZ, Vincent BARLOGIS, Le Guenno GUILLAUME, Vera-Maria HERRMANN, Taco KUIJPERS, Gregoire DUCOUX, Francoise SARROT-REYNAULD, Catharina SCHUETZ, Charlotte CUNNINGHAM-RUNDLES, Frederic RIEUX-LAUCAT, Stuart G TANGYE, Cristina SOBACCHI, Rainer DOFFINGER, Klaus WARNATZ, Bodo GRIMBACHER, Claire FIESCHI, Laureline BERTELOOT, Vanessa L BRYANT, Sophie Trouillet ASSANT, Helen SU, Benedicte NEVEN, Laurent ABEL, Qian ZHANG, Bertrand BOISSON, Aurelie COBAT, Emmanuelle JOUANGUY, Olle KAMPE, Paul BASTARD, Chaim M ROIFMAN, Nils LANDEGREN, Luigi D NOTARANGELO, Mark S ANDERSON, Jean-Laurent CASANOVA and Anne PUEL

Edition

Nature, BERLIN, NATURE PORTFOLIO, 2023, 0028-0836

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30102 Immunology

Country of publisher

Germany

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 64.800 in 2022

RIV identification code

RIV/00216224:14110/23:00133819

Organization unit

Faculty of Medicine

UT WoS

001182780400001

Keywords in English

NF-κB pathway deficiency; I IFNs

Tags

Tags

International impact, Reviewed
Změněno: 8/7/2024 13:49, Mgr. Michal Petr

Abstract

V originále

Patients with autoimmune polyendocrinopathy syndrome type 1 (APS-1) caused by autosomal recessive AIRE deficiency produce autoantibodies that neutralize type I interferons (IFNs)1,2, conferring a predisposition to life-threatening COVID-19 pneumonia3. Here we report that patients with autosomal recessive NIK or RELB deficiency, or a specific type of autosomal-dominant NF-.B2 deficiency, also have neutralizing autoantibodies against type I IFNs and are at higher risk of getting life-threatening COVID-19 pneumonia. In patients with autosomal-dominant NF-.B2 deficiency, these autoantibodies are found only in individuals who are heterozygous for variants associated with both transcription (p52 activity) loss of function (LOF) due to impaired p100 processing to generate p52, and regulatory (I.Bd activity) gain of function (GOF) due to the accumulation of unprocessed p100, therefore increasing the inhibitory activity of I.Bd (hereafter, p52LOF/I.BdGOF). By contrast, neutralizing autoantibodies against type I IFNs are not found in individuals who are heterozygous for NFKB2 variants causing haploinsufficiency of p100 and p52 (hereafter, p52LOF/ I.BdLOF) or gain-of-function of p52 (hereafter, p52GOF/I.BdLOF). In contrast to patients with APS-1, patients with disorders of NIK, RELB or NF-.B2 have very few tissue-specific autoantibodies. However, their thymuses have an abnormal structure, with few AIRE-expressing medullary thymic epithelial cells. Human inborn errors of the alternative NF-.B pathway impair the development of AIRE-expressing medullary thymic epithelial cells, thereby underlying the production of autoantibodies against type I IFNs and predisposition to viral diseases.