Pulmonary autoimmunity as a feature of autoimmune polyendocrine syndrome type 1 and identification of KCNRG as a bronchial autoantigen

Mohammad Alimohammadi(Uppsala University), Noémie Dubois, Filip Sköldberg(Uppsala University Hospital), Åsa Hallgren(Uppsala University Hospital), Isabelle Tardivel, Håkan Hedstrand(Uppsala University Hospital), Jan Haavik(University of Bergen), Eystein S. Husebye(Haukeland University Hospital), Jan Gustafsson(Uppsala University Hospital), Fredrik Rorsman(Uppsala University Hospital), Antonella Meloni(University of Cagliari), Christer Janson(Uppsala University Hospital), B. Vialettes, Merja Kajosaari(University of Helsinki), William Egner(National Health Service), Ravishankar Sargur(National Health Service), Fredrik Pontén(Uppsala University), Zahir Amoura(Sorbonne Université), A Grimfeld(Sorbonne Université), Filippo De Luca(University of Messina), Corrado Betterle(University of Padua), Jaakko Perheentupa(University of Helsinki), Olle Kämpe(Uppsala University Hospital), Jean‐Claude Carel(Inserm)
Proceedings of the National Academy of Sciences
February 27, 2009
Cited by 105Open Access
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Abstract

Patients with autoimmune polyendocrine syndrome type 1 (APS-1) suffer from multiple organ-specific autoimmunity with autoantibodies against target tissue-specific autoantigens. Endocrine and nonendocrine organs such as skin, hair follicles, and liver are targeted by the immune system. Despite sporadic observations of pulmonary symptoms among APS-1 patients, an autoimmune mechanism for pulmonary involvement has not been elucidated. We report here on a subset of APS-1 patients with respiratory symptoms. Eight patients with pulmonary involvement were identified. Severe airway obstruction was found in 4 patients, leading to death in 2. Immunoscreening of a cDNA library using serum samples from a patient with APS-1 and obstructive respiratory symptoms identified a putative potassium channel regulator (KCNRG) as a pulmonary autoantigen. Reactivity to recombinant KCNRG was assessed in 110 APS-1 patients by using immunoprecipitation. Autoantibodies to KCNRG were present in 7 of the 8 patients with respiratory symptoms, but in only 1 of 102 APS-1 patients without respiratory symptoms. Expression of KCNRG messenger RNA and protein was found to be predominantly restricted to the epithelial cells of terminal bronchioles. Autoantibodies to KCNRG, a protein mainly expressed in bronchial epithelium, are strongly associated with pulmonary involvement in APS-1. These findings may facilitate the recognition, diagnosis, characterization, and understanding of the pulmonary manifestations of APS-1.


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