Newest Articles
Adaptive immune responses in Marburg virus survivorsImmune responses that develop in survivors of filovirus infection may indicate critical parameters that could inform rational vaccine development. Stonier et al. characterize immune responses in Marburg virus survivors and demonstrate robust CD4+ T cell responses but limited CD8+ T cell and neutralizing antibody responses.
Platelets as dronesDespite the lack of nuclei and regulated transcription, platelets actively participate in multiple physiological processes, including hemostasis and immunity. Li et al. discuss aspects of platelet design that optimize its functions and argue that platelets may be best conceived as automated, fully equipped surveillance vehicles.
Protein kinase D activates the NLRP3 inflammasomeZhang et al. show that Golgi-mediated protein kinase D (PKD) signaling is required and sufficient for NLRP3 inflammasome activation. PKD at the Golgi phosphorylates NLRP3 to release it from mitochondria-associated endoplasmic reticulum membranes, allowing for assembly of the mature inflammasome in the cytosol.
Increased PD-L1 impairs Th17 in STAT1/3 mutantsZhang et al. show that hyperphosphorylated STAT1 in patients with STAT1 gain-of-function and STAT3 loss-of-function is caused by impaired SOCS3 expression and leads to upregulation of PD-L1 and defects in Th17 cell differentiation that underlie susceptibility to chronic mucocutaneous candidiasis in these patients.
Cooperation between MYD88L265P and CD79BWang et al. show cooperation between MYD88L265P and CD79B mutations dysregulating B cell responses to self-antigen and differentiation into plasma cells. Their results reveal that CD79B and surface IgM constitute a rate-limiting checkpoint against MYD88L265P, explaining the co-occurrence of MYD88 and CD79B mutations in human lymphomas.
Fundamental immunodeficiency and its correctionIn the Kunkel Society Lecture, Nathan calls “fundamental immunodeficiency” the inability of the encoded immune system to protect us from every life-threatening infection. The remedy is “adopted immunity,” including antimicrobial agents. Immunologists can engage with drug developers to help overcome the rising problem of antimicrobial resistance.
Tolerance limits neutralizing HIV-1 antibody responsesSchroeder et al. demonstrate that when peripheral tolerance is relaxed, tier 2 HIV-1–neutralizing antibodies can be elicited and identify new autoreactive antibody specificities against histone H2A capable of neutralizing tier 2 HIV-1.
Role of Blimp-1 in natural Ig secretionThe transcriptional regulator of B cell differentiation, Blimp-1, regulates antibody production by plasma cells after antigen stimulation. Savage et al. demonstrate that spontaneous “natural” IgM and IgG3 production is provided by a heterogeneous set of B-1–derived plasma cells and by B-1 cells; the latter neither express nor require Blimp-1 for maximal antibody production.
Tissues influence fate and function of type 3 ILCsNussbaum et al. found that tumor suppression through innate lymphoid cells (ILCs) cannot be predicted solely based on the ILC phenotype and lineage but that their immune properties are shaped both by their ontogeny and by the tissue microenvironment they reside in.
Notch3 signaling prevents mural cell lossMachuca-Parra et al. show that restoring Notch3 signaling via genetic rescue in a Notch3 knockout or using a Notch3 agonist antibody in a mouse model of CADASIL can prevent small vessel disease.
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October 2, 2017
Volume 214, No. 10
