Innate immune stimulation of whole blood reveals IFN-1 hyper-responsiveness in type 1 diabetes

Kameron Rodrigues (1) , Matthew Dufort (2) , Alba Llibre (3) , Cate Speake (2) , M Jubayer Rahman (1) , Vincent Bondet (3) , Juan Quiel (1) , Peter Linsley (2) , Carla Greenbaum (2) , Darragh Duffy (3) , Kristin Tarbell (1)

1 National Institute of Diabetes and Digestive and Kidney Diseases [Bethesda]
2 BRI - Benaroya Research Institute [Seattle]
3 Immunobiologie des Cellules dendritiques

Self-antigen-specific T cell responses drive type 1 diabetes pathogenesis, but alterations in innate immune responses are also critical and not as well understood. Innate immunity in human type 1 diabetes has primarily been assessed via gene-expression analysis of unstimulated peripheral blood mononuclear cells, without the immune activation that could amplify disease-associated signals. Increased responsiveness in each of the two main innate immune pathways, driven by either type 1 IFN (IFN-1) or IL-1, have been detected in type 1 diabetes, but the dominant innate pathway is still unclear. This study aimed to determine the key innate pathway in type 1 diabetes and assess the whole blood immune stimulation assay as a tool to investigate this.

Mots clés: Enterotoxins; Diabetes mellitus; Cytokines; type 1; Immunity; innate; Interleukin-1; mononuclear; Leukocytes; Monocytes; Type 1 IFN; inbred NOD); Non-obese diabetic mice (mice

Domaines: Immunologie

Kameron Rodrigues, Matthew Dufort, Alba Llibre, Cate Speake, M Jubayer Rahman, et al.. Innate immune stimulation of whole blood reveals IFN-1 hyper-responsiveness in type 1 diabetes. Diabetologia, 2020, ⟨10.1007/s00125-020-05179-4⟩. ⟨pasteur-02860487⟩