A functional polymorphism in IL-36β modulates macrophage antifungal effector functions and increases susceptibility to invasive pulmonary Aspergillosis.

Gonçalves SM, Leite L, de Vasconcelos P, Pereira I, Dewi IMW, Mercier T, Aerts R, Ligeiro D, Mendes F, Freitas F, Condeço J, Vieira J, Espada E, Lagrou K, Maertens JA, Gresnigt MS, Dinarello CA, Lacerda JF, Vaz CP, Cunha C, Carvalho A, van de Veerdonk FL (2025) A functional polymorphism in IL-36β modulates macrophage antifungal effector functions and increases susceptibility to invasive pulmonary Aspergillosis. J Infect Dis [Accepted]

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Abstract

Genetic predisposition plays a major role in the development of invasive pulmonary aspergillosis (IPA). The risk and course of IPA vary significantly among patients, yet continuously new genetic mechanisms that influence individual antifungal immune responses are being discovered. While genetic variability in IL-1 family cytokines is recognized as an important cause of disease susceptibility, it is unclear whether and how less-studied IL-1 family members, such as the IL-36 cytokine subfamily, are genetically regulated and influence the risk of infection.