Abstract not available

Abstract not available

In cancer patients, dendritic cells (DCs) in tumor-draining lymph nodes can present antigens to naive T cells in ways that break immunological tolerance. The clonally expanded progeny of primed T cells are further regulated by DCs at tumor sites. Intratumoral DCs can both provide survival signals to and drive effector differentiation of incoming T cells, thereby locally enhancing antitumor immunity;

The innate immune system is critical for inducing durable and protective T cell responses to infection and has been increasingly recognized as a target for cancer immunotherapy. In this review, we present a framework wherein distinct innate immune signaling pathways activate five key dendritic cell activities that are important for T cell-mediated immunity. We discuss molecular pathways that can agonize

The generation of anti-tumor immunity in the draining lymph nodes is known as the cancer immunity cycle. Accumulating evidence supports the occurrence of such a cycle at tumor sites in the context of chronic inflammation. Here, we review the role of tertiary lymphoid structures (TLS) in the generation of T and B cell immunities, focusing on the impact of B cells that undergo full maturation, resulting

2′3′-cyclic GMP-AMP (2′3′-cGAMP) and 3′2′-cGAMP activate STING-dependent antiviral immunity in Drosophila melanogaster but fail to control infection by C virus in some fly species. In this issue of Immunity, Cai et al. reveal that Drosophila produces multiple cyclic di-nucleotides (CDNs) in response to viral infection. One of these CDNs—2′3′-c-di-GMP—is a very potent STING activator capable of promoting

IL-17-blocking antibodies have shown little clinical effect in some autoimmune diseases such as multiple sclerosis. In this issue of Immunity, Luo et al. demonstrate that SHP2-Act1 complexes can mediate autonomous IL-17R signaling in the absence of the IL-17 ligand itself.

Lymph nodes can be shared among several organs, notably in the gastrointestinal system. In this issue of Immunity, Brown et al. describe how pancreatic immunity is shaped by the mixing of different migratory dendritic cells issued from co-drainage from liver, pancreas, and duodenum.

Many mechanisms by which stress mediates its effects within the central nervous system still remain unknown. Byun, Kim, Kim et al. find that early-life stress triggers corticosterone release to drive astrocyte-dependent synapse elimination and altered behavior. Thus, this work defines a steroid-sensitive astrocyte transcriptional circuit controlling behavior, highlighting how the study of CNS immunoregulation

PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 as a key microglial signaling node and shows that targeting PLCγ2 could have therapeutic benefits in AD

The immune and nervous systems respond to dangerous stimuli to maintain homeostasis. In a recent issue of Nature, Florsheim et al. and Plum et al. uncover the crosstalk between immunoglobulin E (IgE)-mast-cell-mediated immune activation and neural responses driving behavioral avoidance of allergenic food.

Abstract not available

Dendritic cells (DCs) are relatively short lived, yet DC frequencies in lymph nodes are stable. In this issue of Immunity, Ugur et al. reveal that type 1 conventional DCs (cDC1s) are maintained in the deep paracortex of the lymph node from a supply of preDCs that proliferate in nearby medullary vessels. Transition from preDC to cDC1 is regulated by Flt3L sensing.

Whether soluble TREM2 has a functional role in the central nervous system has been unclear. In this issue of Immunity, Zhong et al. show that soluble TREM2 inhibits aberrant synaptic pruning by sopping up the complement factor C1q to protect neurons and mitigate neurodegeneration.

Hypoxia is a major driver of tumor aggressiveness and therapy resistance in GBM. In this issue of Immunity, Sattiraju et al. functionally link hypoxia with diminished anti-cancer immunity caused by sequestration of immunosuppressive TAMs and CTLs in pseudopalisades in GBM.

IL-10 has been linked to COVID-19 severity, but whether it is causal is unclear. In this issue of Immunity, Mitsui et al. find that a specific single-nucleotide polymorphism (SNP) results in expression of an IL10RB-IFNAR2 fusion protein that intensifies IL-10-mediated induction of ACE2 expression and viral infectivity of macrophages.

Communication between the central nervous system and the periphery contributes to stress responses and mood disorders. In a recent issue of Cell, Schneider et al. report that psychological stress exacerbates gut inflammation and dysmotility by modifying enteric glia and neurons.

The enteric nervous system is largely autonomous, and the central nervous system is compartmentalized behind the blood-brain barrier. Yet the intestinal microbiota shapes gut function, local and systemic immune responses, and central nervous system functions including cognition and mood. In this review, we address how the gut microbiota can profoundly influence neural and immune networks. Although

Interleukin-1 (IL-1) is a primary pro-inflammatory cytokine requiring tightly controlled negative regulation. In this issue of Immunity, Wang et al.,1 inspired by an IL-1 receptor missense mutation associated with unleashed IL-1-mediated inflammation, design a new drug to selectively inhibit IL-1.

Interleukin-3 (IL-3) induces emergency hematopoiesis in settings of acute inflammation. In this issue of Immunity, Kiss et al. find that IL-3 derived from astrocytes and CD4+ T cells is a key regulatory cytokine of the central nervous system, and increased IL-3 signaling exacerbates neuroinflammation.

Long-lived plasma cells (LLPCs) play a central role in protective immunity after vaccination and infection. In this issue of Immunity, Robinson, Ding, et al. utilize a timestamping approach to fate map and characterize the LLPC compartment and demonstrate that PC longevity in the bone marrow is independent of competition for niches with newly generated incoming PCs.

Mechanisms of Th1-like Treg suppression are unknown in cancer. Two studies in Immunity by Ayala et al. and Zagorulya et al. demonstrate that Th1-like Treg cells interact with type 1 dendritic cells in tumors and draining lymph nodes to potently suppress anti-tumor immunity.

Memory T cells comprise circulating and tissue-resident subsets. In this issue of Immunity, Evrard et al. generate an imputed high-dimensional, single-cell protein expression atlas of memory CD8+ T cells, providing insights into stable differentiation markers and organ-specific expression patterns.

Innate immunity and the actions of type I and III interferons (IFNs) are essential for protection from SARS-CoV-2 and COVID-19. Each is induced in response to infection and serves to restrict viral replication and spread while directing the polarization and modulation of the adaptive immune response. Owing to the distribution of their specific receptors, type I and III IFNs, respectively, impart systemic