Type I interferonopathies with CNS symptoms

Furthermore, the contribution of signalling through the toll-like receptors versus the cytosolic nucleic acid sensors to induce a strong interferon response is increasingly appreciated, specifically TLR7 signalling in autoinflammatory brain disease. [...]given the weak association between interferon concentrations and clinical phenotypes, analysis of interferon-stimulated genes might turn out to be more useful for diagnosis than analysis of interferon concentrations. [...]the repertoire and understanding of type I interferonopathies is expanding, but many remaining questions render this field attractive for basic and clinical researchers, as well as drug development. AMK has received grants or contracts from German Research Foundation, Einstein Stiftung, Günter Endres Fond, and Federal Ministry of Education and Research (Bundesministerium für Bildung und Forschung); has received consulting fees from Angelini Pharma and Neuraxpharm; has participated on an advisory board for Desitin; and has received support for attending meetings and cenobamate powder for in vitro studies from Angelini Pharma.