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Here the authors show that persistent antigen stimulation drives the generation of CD8+ tissue-resident exhausted T cells with distinct developmental origins, function and therapeutic responsiveness when compared to CD8+ tissue-resident memory T cells.
Here the authors identify adenophages, a previously unknown macrophage population present in exocrine glands in mice and humans. These cells are dependent on ILC2-derived GM-CSF and support glandular homeostasis.
Here the authors show that tissue-resident memory and exhausted T cells in tumors are distinct populations that are shaped by relative presence or absence of TCR signals, suggesting that a tailored therapeutic strategy is needed to target each subset.
Long COVID (LC) involves a spectrum of chronic symptoms after resolution of acute severe acute respiratory syndrome coronavirus 2 infection. Barouch and colleagues show that LC is characterized by persistent activation of chronic inflammatory pathways and T cell exhaustion.
The authors identify a Cys→Ser transformation (C19S) in insulin leading to neoepitope presentation and CD4⁺ T cell autoreactivity in type 1 diabetes. Inflammation and oxidative stress enhanced C19S transformation in β cells and antigen-presenting cells, resulting in C19S-specific CD4⁺ T cells with an activated memory phenotype linked to disease progression.
Klose and colleagues show that the neuropeptide vasoactive intestinal peptide (VIP) acts on LGR5+ epithelial stem cells in the gut to restrain their proliferation and differentiation to secretory cell types. This VIP–VIPR1 interaction acts to limit type 2 immune responses.
Veiga-Fernandes and colleagues show that neuroepithelial interactions differentially control type 1 and type 2 enteric immunity via VIP–VIPR1 signaling.
Nguyen et al. show that the splenic environment provides sequential signals via lymphotoxin and retinoic acid that guide cDC2A development and retention.
In ancestral SARS-CoV-2 infection, NK cell interferon-stimulated gene (ISG)-driven activation correlated with poor antibody breadth. In vitro, NK cell ISG expression boosts cytotoxicity toward TFH-like cells, suggesting a mechanism for impaired antibody responses.
Rutz and colleagues report STK40, a non-catalytic member of the Tribbles pseudokinase family, negatively regulates c-Jun activity during proliferative T cell responses and exhaustion.
