Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Climate change is already affecting vector-borne disease transmission and spread, and its impacts are likely to worsen. In the face of ongoing climate change, we must intensify efforts to prevent and control vector-borne diseases.
Climate change can trigger a sequence of events of significant magnitude with consequences for waterborne diseases. Heavy rainfall, flooding and hot weather are associated with waterborne diseases, but early warning systems could intercept these cascading risks.
Activation of TLR–TRAF6 signaling by chronic inflammation in myelodysplastic syndromes increases the competitive advantage of HSPCs harboring MDS mutations through the upregulation of the ubiquitin-modifying enzyme A20 and a switch from canonical to non-canonical NF-κB signaling.
Single-cell RNA-sequencing of myeloid cells during neuroinflammation identifies a new population of pathogenic Cxcl10-expressing phagocytes, which develop independently of Ly6Chi monocytes but derive from early myeloid precursors shaped by the inflamed tissue microenvironment.
Epigenetic modifications are associated with distinct stages of autoreactive CD8+ T cell differentiation. DNA methylation and chromatin changes guide the acquisition of a memory-like phenotype and sustain prolonged autoimmune effector responses.
Oxidative stress is an imbalance in the production of reactive oxygen species and the ability to remove or detoxify these molecules, which causes cellular damage. Leveraging novel sequencing methods and high-throughput screens leads to the discovery of possible new therapies.
Myeloid-derived suppressor cells (MDSCs) occupy sites of chronic inflammation and suppress CD8+ T cell function. A new study describes the transfer of the metabolite methylglyoxal (MG) to T cells, which mediates this immunosuppressive mechanism.
CD8 memory–phenotype differentiation is a T cell antigen receptor–governed process that begins in Eomes+ thymic precursors and is subsequently completed in the periphery. These CD8-MP cells can infiltrate tumors, where they express PD-1.
The RNA modification N6-methyladenosine (m6A) plays an essential role in the regulation of immunity. Here, Shulman and Stern-Ginossar review the roles of m6A in controlling immune recognition, activation of innate and adaptive immune responses, and cell fate decisions.
Oxidative stress can promote neurodegeneration. Akassoglou and colleagues describe Tox-seq, a functional single-cell RNA sequencing method to identify oxidative stress transcriptional signatures in CNS-resident cells. Tox-seq identified coagulation and glutathione-redox pathway genes that are coupled to oxidative stress and that could be targeted by the glutathione-regulating small molecule acivicin.
Mildner and colleagues characterize two subsets (Cxcl10+ and Saa3+) of monocytes with pathogenic potential in the central nervous system of mice with experimentally induced autoimmune encephalomyelitis and show these pathogenic cells are not derived from Ly6C+ monocytes, but from early myeloid cell progenitors.
Starczynowski and colleagues show that myelodysplastic syndrome HSPCs have a competitive advantage as compared to normal HSPCs during chronic inflammation due to a switch from canonical to noncanonical signaling for the activation of NF-κB.
Therapeutic irradiation can trigger DNA-sensing pathways and trigger antitumor immunity. Fu and colleagues demonstrate that tumors can co-opt intrinsic apoptotic pathways to avoid immunogenic cell death following irradiation.
Myeloid-derived suppressor cells (MDSCs) residing within tumors can impede immune responses. Knolle and colleagues show that MDSCs poison immune cells by producing methylglyoxal, which functionally alters their cellular metabolism and hence their effector responses.
Savage and colleagues show virtual memory CD8 T cells arise in the thymus of replete mice, where their differentiation is a robust TCR-directed process. Clonal analyses show their TCR repertoire is reproducible and distinct from conventional cells and that progeny cells harboring such TCRs infiltrate tumors and express PD-1.
Autoreactive T cells are subject to continuous antigenic stimulation yet sustain their autoreactive functionality. Youngblood and colleagues examine type 1 diabetes systems to show that a pool of autoreactive CD8+ T cells exhibits a stem cell–like signature that facilitates their durable activity.
