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The authors show how Vγ1⁺ γδ T cells produce IL-4 to drive early CD8⁺ T cell and dendritic cell responses to malaria infection in mice.

Here, the authors use a mouse model of multiple sclerosis to show that CD38⁺Foxp3⁺ T_reg cells persist in postinflammatory CNS tissues and are needed for maintaining immune homeostasis. These localized stress-tolerant T_reg cells have developed mechanisms to exploit the limited availability of IL-2 in this tissue.

Phosphorylation-dephosphorylation and ubiquitination tune TCR signaling to avoid self-reactivity. Kim and colleagues show that acetylation also modulates TCR signaling.

FOXP3⁺ regulatory T (T_reg) cells are pivotal for peripheral tolerance and immune suppression. We show that the skin-derived cytokine TSLP promotes GATA3-expressing effector T_reg cells through a specific migratory DC2 subtype derived from transitional dendritic cells whose function requires OX40L, identifying a previously unrecognized tolerogenic axis across contexts of inflammation and cancer.

Treatment-refractory rheumatoid arthritis is a major unmet clinical need, and the mechanisms that underlie resistance to therapy remain poorly understood. Using high-resolution spatial transcriptomics, we identified a spatiotemporal process of fibrogenic remodeling that is associated with failure to respond to treatment.

Comparative single-cell transcriptomic analysis identifies clonally expanded tissue-resident CD8⁺ T cells within the leptomeninges of individuals with neurodegenerative diseases. The findings suggest that this brain border region represents an active immune niche that contributes to neurodegeneration with disease-specific distinctions.

Recent work has revealed that dendritic cells (DCs) are more heterogeneous than previously thought, yet the functional roles of these newly described DC subsets remain unclear. Here, Li et al. find that in mice, TSLP from keratinocytes activates transitional DC-derived DC2 to promote GATA3⁺ regulatory T cells and mediate immunosuppression during inflammation and cancer.

Shinzawa et al. developed CD8^Dual mice that express CD8 co-receptors from both Cd4 and Cd8 gene loci. Using this model they find that thymic distribution of major histocompatibility complex class I peptides influences lineage commitment and CD8⁺ T cell function.

Here the authors show that transient cell cycle arrest reprograms CD8⁺ T cells into a highly energized state, increasing proliferation and antitumor activity and boosting efficacy of immunotherapies in cancer models.

One of three back-to-back papers to show that dosage of BACH2 can modulate T cell differentiation and function and how we might apply this to enhance CAR T cell therapies for cancer.

One of three back-to-back papers to show dosage of BACH2 can modulate T cell differentiation and function and how we might apply this to enhance chimeric antigen receptor T cell therapies for cancer.

One of three back-to-back papers to show that dosage of BACH2 can modulate T cell differentiation and function and how we might apply this to enhance CAR T cell therapies for cancer.

Immune dysfunction and aberrant metabolic remodeling are hallmarks of critical illness including sepsis. Metabolic adaptation of CD4⁺ T cells is now shown to contribute to immunosuppression and poor clinical outcomes in critical illness.

Rathmell and colleagues show that metabolic reprograming of regulatory T cells is associated with severity of critical illness in patients with and without sepsis.

Wei et al. perform spatial transcriptomic profiling on synovial tissue biopsy samples from individuals with recent-onset rheumatoid arthritis, finding TGFβ signaling and fibrogenic fibroblast activation drive a treatment-refractory tissue phenotype.