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AID-NET (Autoinflammatory Syndromes in Children)

Genetics, disease mechanisms, diagnostic markers, and therapeutic targets



We hypothesize that dysregulation of innate immune mechanisms, e.g. alternative secretory pathways, phagocyte activation, reduced anti-inflammatory activities, or dysfunction of PRRs, plays a key role in Autoinflammatory Diseases (AID).


Clinical Registry, Biobanks (DNA/RNA/Serum), and translational projects: In the collaborative clinical research part we will include all patients with AID into a clinical registry and patient material into a DNA/RNA and a serum bank. The patient material will be used for the identification of genetic or serologic markers of the disease. Future use will allow translating the newly discovered pathogenic mechanisms of the innate immune system into feasible tools improving patient care via assessing the potential of novel biomarkers or genetic tests in monitoring disease activity of patients.


Autoinflammatory syndroms (CINCA, MWS, FMF, TRAPS, SOJIA) as well as PFAPA and clinically defined AID diseases


Dr. med. Ulrich Neudorf

Dr. med. Elke Lainka
E-Mail: Telefonsprechstunde Do 13:30-14:00
Telefon: 0201 723-3632
Fax: 0201 723-5394

Prof. Dr. med. Tim Niehues
E-Mail: HELIOS-Klinikum Krefeld
Lutherplatz 40
47805 Krefeld

Aktueller Stand

Das Projekt ist abgeschlossen.