Search

A study in Science Immunology reports that regulatory T cells in the skin modulate neuronal tone directly through their production of the opioid enkephalin.

A study by Bhattarai et al. in Nature Immunology reports that ILC3-to-ILC1 plasticity in the gut is regulated by circadian clock proteins.

Increased intratumoral acidity associated with a high-fat diet accelarates tumour growth through the acid-sensing receptor GPR65 on tumour-associated macrophages.

Thierry, Baudon et al. show that non-classical monocytes are nurtured by endothelial cell expression of CSF1 throughout the whole vascular tree.

A study in Nature reports a lactate–HIF1α–NDUFA4L2 pathway in intestinal dendritic cells that regulates the inflammatory priming of encephalitogenic T cells.

Wei et al. report a role for membrane perforation mediated by gasdermin D pores in disruption of the blood–brain barrier.

Glycosylated RNAs on the surface of neutrophils bind P-selectin on endothelial cells to mediate recruitment to sites of inflammation.

Liver X receptor (LXR) signalling can inhibit the DNA-sensing cGAS–STING inflammatory pathway through degradation of the second messenger cGAMP.

In contrast to its role in promoting immune responses to viral and bacterial infections, STING inhibits SYK-dependent cytokine production in response to fungal infection.

Gillian Griffiths and colleagues show that T cell receptor downregulation at the immune synapse occurs through ectocytosis, which terminates receptor signalling and promotes dissociation from target cells.

A study in Immunity reports that a high-fat diet in mice leads to the loss of PPARγ⁺ T_reg cells in the skin, which exacerbates psoriasis mediated by IL-17-producing γδ T cells.

Two studies published in Nature report that gasdermin-mediated pyroptosis of tumour cells induces cytotoxic lymphocyte-mediated antitumour immune responses.

Histone deacetylases are typically involved in transcriptional repression, but a report in Nature describes a mechanism by which HDAC3 can also activate macrophage transcription in response to lipopolysaccharide in a deacetylase-independent manner.

Overexpression of JUN by CAR T cells renders them resistant to exhaustion and improves tumour control in mouse models, including of solid tumours and of tumours with low levels of antigen expression.

Liver macrophages produce the non-inflammatory factor IGFBP7, which has direct effects on liver metabolism in metabolic disease without requiring a switch to a pro-inflammatory phenotype.

White et al. show that microbiota-specific T cells are licensed by gut inflammation to infiltrate the central nervous system, where cross-reactivity with self-antigens leads to neuropathology.

Although the aryl hydrocarbon receptor has an essential role in supporting homeostasis of intestinal intraepithelial lymphocytes, its activation must be regulated to prevent oxidative stress and death of these cells.

A paper in Cell describes a role for regulatory T cells in mediating the symptoms of opioid withdrawal through effects on neuronal synapses.

Accumulation of inhaled carbon particulates in lung-draining lymph nodes with age impairs respiratory immunity.

Under conditions of endoplasmic reticulum stress, tumour cells release cholesterol-containing extracellular vesicles that promote the immunosuppressive functions of myeloid-derived suppressor cells.

Cross-talk between stromal cells and T helper 2 cells in adipose tissue supports anti-parasite immune responses.

Clusters of quiescent cancer cells in triple-negative breast cancer create an immunosuppressive microenvironment that might contribute to immunotherapy resistance and tumour recurrence.

Diurnal rhythmicity of IgA production by intestinal plasma cells is entrained by time of feeding, with effects on composition and metabolic activity of the commensal microbiota.

Intestinal ILC3s produce the epidermal growth factor family mediator HB-EGF, which protects the intestinal barrier against TNF-induced epithelial cell death.

Wattrus et al. report a role for embryonic macrophages in zebrafish in promoting the death or proliferation of haematopoietic stem cells (HSCs), which regulates HSC clonality into adulthood.

IL-17 production by skin-resident γδ T cells is required for optimal HIF1α activation in damaged epithelium, leading to epithelial cell migration and re-epithelialization.

New research shows that red blood cells express surface TLR9 that binds cell-free DNA, leading to erythrophagocytosis and innate immune activation.

A recent study in Immunity describes that mast cells can degranulate directly into the bloodstream to prime neutrophils for rapid extravasation at sites of tissue inflammation.

A recent study in Science describes how the innate immune sensor cGAS is inhibited by phosphorylation during mitosis to prevent an inflammatory response to self-DNA.

Sussan Nourshargh and colleagues outline a mechanism for the reverse transendothelial migration of neutrophils that they observe occurs more frequently in aged mice than in young mice.

This study reports serum metabolome profiling of children naturally infected with Plasmodium falciparum in Burkina Faso, West Africa, revealing major changes in endogenous steroid levels with effects on adaptive immunity.

New research published in Immunity suggests that the increased rigidity of cancer cells during metastasis can result in a biophysical vulnerability to killing by cytotoxic lymphocytes through a form of mechanosurveillance.

Five recent papers identify the RORγt⁺ antigen-presenting cells that induce food-antigen-specific regulatory T cells and establish food tolerance.

The angiogenic growth factor placental growth factor is produced by T_H17 cells and induces T_H17 cell differentiation, which suggests a positive feedback loop between angiogenesis and autoimmunity in chronically inflamed tissues.

The response to anti-PD1 therapy depends on the expression of CXCR3 ligands by dendritic cells in the tumour, which promote the proliferation and activation of intratumoural CD8⁺ T cells.

Stimulation of cutaneous TRPV1⁺ neurons is sufficient to induce a type 17 inflammatory response that spreads to surrounding skin areas to provide ‘anticipatory’ host defence against fungal infection.

Multi-omics profiling of endothelial cells, epithelial cells and fibroblasts from 12 mouse organs was used to create an atlas of immune gene activity in structural cells.

This study supports the suspected autoimmune nature of narcolepsy by showing that patients have memory T cells targeting self-antigens expressed by hypocretin neurons.

Commensal bacteria at mucosal surfaces can remotely control the thymic maturation of mucosal-associated invariant T cells through the production of microbial factors that enter the circulation and are taken up by thymic cells.

This study describes a mechanism of tumour immune evasion through post-translational chemokine modification by dipeptidyl peptidase 4, which inhibits eosinophil-mediated antitumour responses.

This study identifies a role for group 3 innate lymphoid cells in IL-2 production in the small intestine to maintain intestinal homeostasis through effects on regulatory T cells.

The antiviral protein viperin catalyses the production of a small molecule inhibitor of viral RNA polymerization.

Levels of CCR5 expression by CD4⁺ T cells, which influence the outcome of HIV-1 infection, are modulated by polymorphism of a non-coding RNA that affects mRNA stability.

Using spiky microparticles, the authors show that physical cues, such as topological features on the surface of a pathogen, can trigger an immune response by exerting mechanical stress on immune cells.

Chen Dong and colleagues describe a positive-feedback loop between TOX2 and BCL-6 that helps to drive the development of T follicular helper cells in germinal centres.