About the Authors

Anthony Meager

To whom correspondence should be addressed. E-mail: ameager@nibsc.ac.uk

Affiliation Biotherapeutics, National Institute for Biological Standards and Control, South Mimms, United Kingdom

Kumuthini Visvalingam

Affiliation Biotherapeutics, National Institute for Biological Standards and Control, South Mimms, United Kingdom

Pärt Peterson

Affiliation Molecular Pathology, Institute of General and Molecular Pathology, Biomedicum, University of Tartu, Tartu, Estonia

Kaidi Möll

Affiliation Molecular Pathology, Institute of General and Molecular Pathology, Biomedicum, University of Tartu, Tartu, Estonia

Astrid Murumägi

Affiliation Institute of Medical Technology, University of Tampere, Tampere, Finland

Kai Krohn

Affiliation Institute of Medical Technology, University of Tampere, Tampere, Finland

Petra Eskelin

Affiliations Department of Human Molecular Genetics, National Public Health Institute, Helsinki, Finland , Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland

Jaakko Perheentupa

Affiliation Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland

Eystein Husebye

Affiliations Division of Endocrinology, Institute of Medicine, University of Bergen, Norway , Department of Medicine, Haukeland University Hospital, Bergen, Norway

Yoshihisa Kadota

Address ¤ Current address: Toneyama National Hospital, Osaka, Japan

Affiliation Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom

Nick Willcox

Affiliation Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom

Competing Interests

The authors have declared that no competing interests exist.

Author Contributions

A. Meager, P. Peterson, and N. Willcox initiated and designed the study. A. Meager, K. Visvalingam, P. Peterson, K. Möll, A. Murumägi, K. Krohn, P. Eskelin, J. Perheentupa, Y. Kadota, E. Husebye, and N. Willcox collected samples or data or did experiments for the study. K. Möll cultured monocyte-derived DCs from the APS1 patients' and healthy donors' blood, and extracted total RNA and synthesized cDNA, which was used in the quantitative RT-PCR experiment. A. Meager, P. Peterson, K. Möll, J. Perheentupa, and N. Willcox analyzed the data. P. Eskelin designed and performed mutational analyses and human leukocyte antigen genotyping of the APS1 patients. J. Perheentupa and E. Husebye enrolled Finnish and Norwegian APS1 patients, respectively. K. Krohn enrolled the APS1 patient whose peripheral blood monocytes were used by K. Möll to generate DCs. J. Perheentupa and E. Husebye are the clinicians who followed all the APS1 patients involved, collected and organized all the clinical data defining each individual's course of disease, enrolled them for the study of the immune pathology of APS1, stored all the serum samples that were analyzed in this study, participated in the analysis of the immunological versus the clinical findings, and contributed to the revision of the manuscript at several stages. P. Peterson and N. Willcox collected serum samples from patients with APS2, or sporadic CMC, HP, or AD. N. Willcox also helped to collect the samples from the MG/thymoma patients mentioned in Table 2. A. Meager and N. Willcox played a major role in drafting the text, and P. Peterson, K. Möll, K. Krohn, J. Perheentupa, and E. Husebye contributed to writing the paper.