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Cohousing pet-store mice with laboratory mice leads to the natural transfer of microbes and subsequent inflammation in laboratory mice. Lung group 2 innate lymphoid cells — rapid responders to airway allergens — are transiently inhibited by inflammatory signals, but their activity recovers once the active infection subsides.
The bacillus Calmette–Guérin (BCG) vaccine induces homotypic protection against tuberculosis and, surprisingly, heterotypic protection against other pathogens. New work shows that BCG vaccination causes leakage of microbial gut metabolites into circulation, which induces changes in alveolar macrophages protective against pneumonia.
The US National Institute of Allergy and Infectious Diseases (NIAID) convened a virtual workshop in July 2022 to address the research landscape and identify gaps and opportunities in the understanding of durable vaccine protection.
Haimon et al. examine the function of microglia in a relapsing–remitting mouse model of multiple sclerosis, finding that these cells preferentially interact with regulatory T cells compared with effector T cells, and that these cognate interactions require interferon-γ signaling and are critical to maintain regulatory T cell activity.
Based on the identification of CD4+ T cell clones specific for distinct epitopes in the SARS-CoV-2 proteins, Long and colleagues characterize how mutations in these epitopes lead to loss of recognition by the CD4+ T cells elicited by natural infection or vaccination.
Parenteral BCG vaccination has been shown to drive innate immune memory responses that can affect the response to pathogens other than mycobacteria. Here the authors show an innate immune memory mechanism whereby subcutaneous BCG vaccination alters the intestinal microbiome and in turn can train alveolar macrophages in the lungs.
Gringhuis and colleagues show that the extent of type I IFN responses induced by fungal stimulation in human DCs modulate the activation of TGF-β and the production of pathogenic or non-pathogenic TH17 cells.
Understanding immune determinants of vaccine-mediated immunogenicity could further provide rational vaccine design. Two research groups revealed pre-existing and early innate immune signatures associated with better vaccine-mediated antibody responses.
A dogma in the inflammasome field is that NLRP3 activation occurs at dispersed vesicles of the trans-Golgi network. Here, Ricci and colleagues find that these vesicles are of endosomal origin and that endosomes comprise the compartment where NLRP3 is activated.
Mechanisms that explain the hygiene hypothesis for allergy and asthma are unclear. A mouse model that cohouses ‘dirty’ pet-store mice with clean laboratory mice might help to understand this immunology.
Yang and colleagues report that MAIT cells are present in the meninges where they play an essential role in repressing tissue ROS accumulation and preserving meningeal barrier integrity.
Halper-Stromberg and Jabri discuss the molecular and functional adaptations to inflammatory or pathogenic stimuli that shape the immune identity of each individual.
Here the authors show that mice exposed to a variety of pathogens initially have impaired innate type 2 responses to lung allergens, but reactivity resets over time, indicating that microbial experience does not stably inhibit innate immunity to allergens.
By combining single-cell mRNA sequencing and a genetic pulse–chase mouse model, we identified multiple subsets of mouse long-lived plasma cells and showed that these cells can originate from diverse developmental routes.
A stage-specific enhancer augments Notch1 signaling from the early thymic progenitor (ETP) through double-negative thymocyte stages. Enhanced Notch1 activity is required for T cell lineage differentiation at the later end of this developmental interval, but Notch1 also suppresses precocious T lineage commitment in ETPs and promotes their expansion as multi-lineage progenitors.