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The identification of IRAK2 deficiency reveals how impaired Myddosome signalling can paradoxically promote interferon-driven inflammation, which expands the spectrum of monogenic immune dysregulation and underscores the importance of detecting structural variants in unsolved inborn errors of immunity.
The 21st International Aegean Conference on Innate Immunity showcased advances that position innate immunity as a multiscale regulatory system integrating environmental, metabolic, epigenetic and genetic inputs.
Tsiartas and Bennett discuss the discovery that atheroclerotic plaque vulnerability to rupture arises from the interaction between plaque composition and vessel biomechanics.
The identification of IRAK2 deficiency reveals how impaired Myddosome signalling can paradoxically promote interferon-driven inflammation, which expands the spectrum of monogenic immune dysregulation and underscores the importance of detecting structural variants in unsolved inborn errors of immunity.