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The resolution of inflammation is a protective response. The identification and characterization of new players that boost this response might inform the development of novel therapies for non-resolving inflammatory diseases.
While important evidence for the role of myeloid cells in myocardial infarction has accumulated in recent years, single-cell transcriptomics fully delineates the functional heterogeneity of the myeloid cell compartment.
The mechanism of action of the lymphocyte checkpoint protein LAG-3 was always rather mysterious. It now seems to operate at least in part by recognizing and suppressing responses to stable complexes of peptide and major histocompatibility complex class II.
Transcription factors orchestrate stage-specific gene expression during development. Two such factors, TCF-1 and HEB, collaborate at the protein and genomic levels to regulate gene expression in developing thymocytes.
A new model proposes that an applied force allows the co-receptor CD8 and the kinase Lck to selectively stabilize TCR interactions with negatively selecting ligands, but not those with positively selecting ligands, during the negative selection of self-reactive thymocytes.
Acidic microenvironments induced by highly glycolytic tumor cells promote the noninflammatory polarization of tumor-associated macrophages, which leads to immunoevasion.
Deposition of fibrin in the brain and central nervous system occurs after injury or disease. This process unmasks a conserved cryptic epitope of fibrin that activates microglia; blocking this interaction can limit inflammation and neurotoxicity.
Arginine methylation is a post-translational modification that controls the abundance of γc cytokine receptor on mature T cells by a post-transcriptional mechanism.
An antibody to dengue virus that lies flat on its target, neutralizes the virus and also prevents antibody-dependent enhancement of infection is now identified.
Studies of mice demonstrate a link between the female hormone estrogen and protection against bacteremia and sepsis through the induction of natural antibodies to Eshcerichia coli.
Cell-type-specific regulation of gene expression by transcription factors is a fundamental principle of biology. New findings show that microRNA-mediated control of target-gene expression is also dependent on the cellular context.
New insights into how NK cells are educated by the receptor NKG2D, which leads to effects on another receptor, NCR1, raise interesting questions about why so many receptors are linked to the education of NK cells.
Group 2 innate lymphoid cells (ILC2s) that produce the cytokine IL-5 are found in lung, gut, fat and skin tissues. New findings indicate that ILC2s in different tissues selectively express distinct functional cytokine receptors for cell activation in response to the local environment.
Immune responses have the potential to induce life-threatening conditions. A novel multi-system pathway in which neuroendocrine signaling induces expression of the checkpoint receptor PD-1 on NK cells is an important mechanism for protection against cytokine-mediated disease during viral infection.
In the current issue of Nature Immunology, Casanova and colleagues demonstrate that humans (and mouse models) with autosomal-recessive SPPL2a deficiency have a severe defect in conventional dendritic cell 2 survival and production of IL-12 and IL-23, and diminished IFN-γ secretion by mycobacterium-specific memory T cells, thus resulting in increased susceptibility to mycobacterial diseases.
Single-cell transcriptomic analysis shows that B cells experience a continuum of cyclic transitional states during the germinal center (GC) reaction; this pattern is lost in GC-derived follicular lymphoma cells, which seem to be heterogeneous and desynchronized.
Chronic infection with human immunodeficiency virus impairs B cell antigen receptor signaling via a newly described mechanism of inhibitory signaling mediated by IgG3 and the IgG Fc receptor FcRγIIb (CD32b).
