In the current issue of Nature Immunology, Casanova and colleagues demonstrate that humans (and mouse models) with autosomal-recessive SPPL2a deficiency have a severe defect in conventional dendritic cell 2 survival and production of IL-12 and IL-23, and diminished IFN-γ secretion by mycobacterium-specific memory T cells, thus resulting in increased susceptibility to mycobacterial diseases.
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Acknowledgements
This work was supported by the Intramural Research Program, NIH Clinical Center, US National Institutes of Health (NIH). The content of this article does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US government.
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Rosenzweig, S.D. Old vaccines, new diseases: when BCG meets SPPL2a. Nat Immunol 19, 906–907 (2018). https://doi.org/10.1038/s41590-018-0193-0
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DOI: https://doi.org/10.1038/s41590-018-0193-0
