A biallelic mutation in IL6ST encoding the GP130 co-receptor causes immunodeficiency and craniosynostosis

نویسندگان

  • Tobias Schwerd
  • Stephen R F Twigg
  • Dominik Aschenbrenner
  • Santiago Manrique
  • Kerry A Miller
  • Indira B Taylor
  • Melania Capitani
  • Simon J McGowan
  • Elizabeth Sweeney
  • Astrid Weber
  • Liye Chen
  • Paul Bowness
  • Andrew Riordan
  • Andrew Cant
  • Alexandra F Freeman
  • Joshua D Milner
  • Steven M Holland
  • Natalie Frede
  • Miryam Müller
  • Dirk Schmidt-Arras
  • Bodo Grimbacher
  • Steven A Wall
  • E Yvonne Jones
  • Andrew O M Wilkie
  • Holm H Uhlig
چکیده

Multiple cytokines, including interleukin 6 (IL-6), IL-11, IL-27, oncostatin M (OSM), and leukemia inhibitory factor (LIF), signal via the common GP130 cytokine receptor subunit. In this study, we describe a patient with a homozygous mutation of IL6ST (encoding GP130 p.N404Y) who presented with recurrent infections, eczema, bronchiectasis, high IgE, eosinophilia, defective B cell memory, and an impaired acute-phase response, as well as skeletal abnormalities including craniosynostosis. The p.N404Y missense substitution is associated with loss of IL-6, IL-11, IL-27, and OSM signaling but a largely intact LIF response. This study identifies a novel immunodeficiency with phenotypic similarities to STAT3 hyper-IgE syndrome caused by loss of function of GP130.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Oncogenic deletion mutants of gp130 signal from intracellular compartments.

Interleukin 6 (IL-6) and, hence, activation of the IL-6 receptor signalling subunit glycoprotein 130 (gp130; also known as interleukin-6 receptor subunit β, IL6ST), has been linked to inflammation and tumour formation. Recently, deletion mutations in gp130 have been identified in inflammatory hepatocellular adenoma. The mutations clustered around one IL-6-binding epitope and rendered gp130 cons...

متن کامل

Biochemical and functional analyses of gp130 mutants unveil JAK1 as a novel therapeutic target in human inflammatory hepatocellular adenoma

Inflammatory hepatocellular adenomas (IHCAs) are benign liver lesions that can be characterized histologically by the presence of an inflammatory infiltrate and at the molecular level by the overexpression of acute phase inflammatory response genes. Recurrent somatic mutations of the interleukin-6 (IL-6) signal transducer (IL6ST) locus, encoding the critical component of the IL-6 signal transdu...

متن کامل

Signal transducer of inflammation gp130 modulates atherosclerosis in mice and man

Liver-derived acute phase proteins (APPs) emerged as powerful predictors of cardiovascular disease and cardiovascular events, but their functional role in atherosclerosis remains enigmatic. We report that the gp130 receptor, which is a key component of the inflammatory signaling pathway within hepatocytes, influences the risk of atherosclerosis in a hepatocyte-specific gp130 knockout. Mice on a...

متن کامل

Mutations in the Basal Core Promoter and Precore/Core Regions of Hepatitis B Virus in Patients Co-Infected With Human Immunodeficiency Virus

ABSTRACT          Background and objectives: Globally, about one third of the population has been infected with Hepatitis B virus (HBV) and more than 400 million people have become chronically infected. Nearly, 20-25% of all carriers develop serious liver diseases such as cirrhosis, chronic hepatitis and hepatocellular carcinoma (HCC). According to t...

متن کامل

A Novel Mutation in Exon 4 of the Low Density Lipoprotein (LDL) Receptor Gene in an Iranian Familial Hypercholesterolemia Patient

Familial hypercholesterolemia (FH) is an autosomal co-dominant disorder of lipid metabolism, caused by mutations in LDL receptor gene. The penetrance of FH is almost 100%, meaning that half of the offspring of affected parents born with disease. The patients are at risk of premature coronary heart disease (CHD). There is no report about the molecular basis of FH in Iran. Identification of mutat...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 214  شماره 

صفحات  -

تاریخ انتشار 2017