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The transcription factor NFAT5 regulates T cell exhaustion, a dysfunctional state caused by chronic exposure to antigen and other signals, during cancer but not during chronic viral infection.
Verdeil and colleagues show that the transcription factor NFAT5 is selectively required in tumor-induced, but not chronic infection-induced, CD8+ T cell exhaustion, possibly due to the modulation of NFAT5 activation by hyperosmolarity in the tumor environment.
Iron metabolism has been shown to play an important role in the development and function of the immune system, but its role in ILC3s is unclear. Here the authors show that CD71-mediated iron metabolism controls ILC3 proliferation and the host response to Citrobacterrodentium infection and CD71 expression is regulated by Ahr signaling.
IRF4 is required for the differentiation of T cells, B cells and some myeloid cells. A new study finds that IRF4 is upregulated following natural killer (NK) cell activation and is required for the differentiation and expansion of virus-specific NK cells by controlling nutrient acquisition, including iron uptake.
Santosa et al. show that IRF4 is upregulated upon NK cell activation and acts as a signal integrator for the differentiation and expansion of mouse cytomegalovirus-specific NK cells by partly controlling nutrient uptake required for adaptive NK cell responses.
A recent study identified a microglia–T cell communication axis that retains CD8+ T cells in brains with amyloid pathology. Data from this study indicate that CD8+ T cells restrict Alzheimer’s disease pathogenesis.
Chi and colleagues identify brain-resident CXCR6+PD-1+CD8+ T cells that interact with resident microglia to limit immune-mediated pathology in a mouse model of Alzheimer’s disease.
Glioblastoma is a devastating primary brain tumor consisting of multiple cell populations. We identified TFPI2 as the crucial effector of the symbiotic interaction between glioblastoma stem cells and microglia. Blockade of this symbiosis inhibited tumor growth and synergized with an immune checkpoint inhibitor in mouse models of glioblastoma.
Proal and colleagues review the evidence for long-term persistence of coronavirus SARS-CoV-2 in tissues of infected individuals and discuss how this viral reservoir may contribute to the pathogenesis of post-acute sequelae of COVID-19 (PASC).
Here the authors show that TFPI2 promotes glioblastoma stem cell self-renewal and connects stemness to microglia immunosuppression, plus targeting TFPI2-mediated glioblastoma stem cell–microglia symbiosis inhibits tumor growth and synergizes with anti-PD1 therapy in glioblastoma.
Zikherman and colleagues uncover a new mechanism by which B cells recognize virus-like antigen display as a stand-alone danger signal (independent of nucleic acid cargo) that does not rely exclusively on avidity and BCR cross-linking.
Control of the alternative commitment of immature CD4+CD8+ T cells to the CD4+ or CD8+ lineage has long been the subject of intense scrutiny. A combination of CITE-seq and functional assays provides significant new insights into the distinct T cell antigen receptor signaling requirements for these lineage fates.
A recent study shows how intratumoral glutamine supplementation can improve the function of tumor-infiltrating dendritic cells and enhance the CD8+ T cell anti-tumor response.