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Delineation of the steps that lead to immune-related adverse effects indicates that checkpoint-mediated suppression of autoreactive T cells occurs within peripheral target tissues rather than at the point of lymph node activation.
Despite the absence of MHC class II molecules on tumor cells, stem-cell-like CD4+ T cells specific for tumor neoantigens can mediate profound antitumor effects by licensing antigen-presenting cells and augmenting antitumor CD8+ T cells in the tumor microenvironment and draining lymph nodes.
Confusion exists as to whether transitional dendritic cells are a bone fide subset or just a transitional state, as the name indicates. New data are complicating matters further by showing some interesting heterogeneity in these cells.
CD8+ virtual memory T cells have been studied mainly for their antimicrobial functions but it seems that their descendants can contribute to inflammation and hair loss in the context of alopecia areata.
Naive B cells activated during infection enter the germinal center (GC) reaction, in which high-affinity antibodies are generated. A new study has uncovered a distinct metabolic requirement for B cells poised to undergo the GC reaction, whose activation required lactate dehydrogenase A-dependent aerobic glycolysis.
COVID-19 vaccines have been successful, but their duration and level of protection could be improved to cover all SARS-CoV-2 variants. A self-assembling enveloped virus-like particle vaccine combining features of mRNA and protein vaccines might provide a way forward.
Single-cell RNA sequencing distinguishes subsets of fibroblastic reticular cells and predicts pathways that support immune function via crosstalk with lymphocytes.
Presentation of signal peptides by HLA-E to natural killer cells prevents cell lysis via interactions with the inhibitory CD94–NKG2A receptor. A study now reveals an unexpected level of sophistication and heterogeneity in this receptor–ligand interaction.
Indigenous populations are disproportionately affected by COVID-19, but are rarely studied. An investigation of the immune response of Australian First Nations people to SARS-CoV-2 vaccination and infection shows a major effect of comorbidities.
In mice and humans, changes in neutrophil phenotypes and functionality during aging aggravate thromboinflammation in ischemic brain injury and determine the pathology associated with strokes. In mice, inhibition of CXCL3 signaling and rejuvenation of bone marrow offer ways of restricting brain injury and improving stroke outcomes.
Bystander activation that leads to expression of IL-9 in effector TH9 cells is induced by a TCR-independent, STAT-dependent mechanism and may represent a new strategy for therapeutic intervention to treat TH9-induced pathologies in vivo.
Deletion of TFAM, the master regulator of mitochondrial transcription and translation, limits germinal center reactions. Notably, TFAM affects several processes beyond bioenergetics, such as migration, signaling, somatic hypermutation and redox balance.
New work from Udeochu, Amin, Huang, and colleagues provides mechanistic insights into how the tau protein engages the cGAS–STING pathway to elicit antiviral responses in Alzheimer’s disease. This signaling axis diminishes the MEF2C transcriptional network in neurons critical for maintaining cognitive function.
Orthogonal engineering of adoptively transferred CD8+ T cells to co-express two cytokines — an IL-2Rβ/γ-biased IL-2 variant and the proinflammatory alarmin IL-33 — induces an exhaustion-resistant synthetic cell state with potent anti-tumor efficacy in the absence of host pre-conditioning.
APLAID is a very rare autoinflammatory disease thought to be caused by mutations in PLCG2. A mouse model of APLAID recapitulates clinical features of the disease, and identifies a crucial function for G-CSF that might be targeted therapeutically.
The immune system is not immune to sex differences. New research now uncovers the molecular mechanisms that underlie sex-based differences during antiviral immune responses.
Mononuclear phagocyte proliferation is thought to be limited to myeloid progenitor cells and mature macrophages. However, availability within an interstitial macrophage niche permits the proliferation of monocytes in the lung before macrophage differentiation.
Capturing cell organization in the tumor microenvironment using spatial proteomics can provide insight into the disease. A pair of studies applying this to advanced lung and brain tumors identifies organizational immune hallmarks that are associated with patient outcomes.
Antibody dynamics resulting from sequential immunization are complex, limiting the study of concepts such as ‘original antigenic sin’. Here, molecular fate-mapping defines an ‘addiction’ of boosted antibodies to primary clones, and OAS-like suppression of new clones, to a degree inversely related to boosting antigenic distance.
