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Mucosa-associated invariant T (MAIT) cells recognize vitamin B metabolites presented by the molecule MR1. Rossjohn and colleagues generate multiple altered metabolite ligands and determine their structures in the context of MR1 and the TCR to develop a generalized framework for MAIT cell antigen recognition.
Immunological memory is a crucial feature of adaptive immunity. A new report proposes a novel ‘outside-in’ mechanism by which a recall immune response may be initiated from the tissue, rather than secondary lymphoid organs.
Comprehensive analysis of CD8+ T cell populations specific to cytomegalovirus reveals that the evolution of the T cell antigen receptor repertoire during chronic infections is characterized by the expansion of low-affinity clones.
The ubiquitin-editing enzyme A20 has a pivotal role in restricting autoimmune and inflammatory responses. New studies suggest that A20 prevents inflammatory diseases using a non-catalytic mechanism involving ubiquitin binding.
γδ T cells are critical contributors to tissue homeostasis. Recent research identifies an unexpected role for γδ T cell–derived IL-17F in promoting sympathetic innervation and tissue thermogenesis through the induction of the cytokine TGF-β in adipose cells.
Turley and Krishnamurty review new insights into lymph node stromal cells, a heterogeneous cell population that serves distinct functions during development, in maintaining lymphocyte homeostasis, and in coordinating immune responses.
van Loo and colleagues provide insights into the action of the anti-inflammatory protein A20. The ZnF7 and ZnF4 ubiquitin-binding domains of A20 are both required to suppress inflammatory signaling and cell death; however, these zinc fingers operate via distinct mechanisms.
Monticelli and colleagues analyze primary human CD4+ T cells to interrogate gene expression regulatory pathways that distinguish GM-CSF+ pathogenic programs from noninflammatory programs. They identify the transcriptional repressor BHLHE40 as an enforcer of proinflammatory gene expression by suppressing the NF-κB inhibitor miR-146a and the RNase ZC3H12D.
Mucosal-associated invariant T (MAIT) cells recognize vitamin B metabolites presented by the molecule MR1. Rossjohn and colleagues generate multiple altered metabolite ligands and determine their structures in the context of MR1 and the TCR to develop a generalized framework for MAIT cell antigen recognition.
Tissue-resident memory (TRM) cells are generally stably maintained in discrete tissues or organs. Masopust and colleagues show that TRM cells can reenter the circulation, and exhibit considerable plasticity, although they retain a proclivity to reestablish themselves in their tissue of origin.
The deubiquitinase A20 is a potent inhibitor of NF-κB signaling pathways. Ma and colleagues identify distinct roles for A20 ubiquitin-binding ZF4 and ZF7 domains, which exhibit different phenotypes upon mutation, but play synergistic roles in regulating inflammatory responses.
Busch and colleagues use single-cell and bulk TCR sequencing and structural affinity analyses of CMV-specific T cells to show that the immunodominance of high-affinity T cell clones declines during chronic infection with CMV, likely due to cellular senescence.
PD-L1 on tumor cells exerts an important dampening effect on T cells via their expression of PD-1. Miller and colleagues find that PD-L1 ‘back-signaling’ into T cells and macrophages can also dampen immune responses within the tumor microenvironment.
Unanue and colleagues examine the immunopeptidome of pancreatic islets in non-obese diabetic (NOD) mice, which spontaneously develop autoimmune diabetes, to reveal the key features of a restricted component in the self-MHC-II peptidome that causes autoreactivity.
The pathobiological validity of mouse models of mycobacteria infection is sometimes questioned. O’Garra and colleagues demonstrate that mice share transcriptomic modules with active human tuberculosis and a characteristic type I IFN signature.