Reviews & Analysis

A previously unknown role is identified for a pathway that involves major histocompatibility complex class I and an inhibitory receptor, LILRB1, that regulates the phagocytosis of cancer cells by macrophages and contributes to resistance directed against the signal-regulatory protein CD47.

A new ‘alarm mechanism’ of the innate immune system that signals the presence of nuclear viruses involves the sensing of host 5S rRNA by RIG-I.

Single-cell sequencing identifies novel subtypes of intestinal epithelial cells and their molecular signatures, which reveals new principles for gut homeostasis and the response to infection.

Damaged mitochondria are targeted for mitophagy by the Pink–Parkin ubiquitin pathway. The mitochondrial ATPase Atad3a prevents aberrant activation of Pink and protects hematopoietic stem cells.

Emerging viral diseases present a huge and increasingly important global threat to public health systems. Graham and Sullivan discuss the challenges presented by emerging viral diseases and discuss how innovations in technology and policy can address this threat.

Nikolich-Žugich reviews recent developments in our understanding of age-related changes affecting key components of immunity

Adenosine produced by apoptotic regulatory T cells (T_reg cells) has a more important immunosuppressive role in the tumor microenvironment than that of live T_reg cells. This discovery raises the possibility of novel strategies for cancer immunotherapy.

Abolishing signals mediated by the inhibitory receptor PD-1 results in a systemic decrease in tryptophan and tyrosine, which leads to a striking deficiency in the neurotransmitters serotonin and dopamine in the brain and anxiety-like behavior and exacerbated fear.

Replacement of resident alveolar macrophages by monocyte-derived macrophages after herpesvirus infection protects against asthma.

Mucosal-associated invariant T cells (MAIT cells) normally preserve gut-barrier integrity but can switch their phenotype to have a pathogenic role in type 1 diabetes.

Lambris and colleagues discuss new and previously unanticipated functions of complement and how these affect immunity and disease pathogenesis.

Dysfunctional immunity is associated with dengue hemorrhagic fever and dengue shock syndrome. Structural analyses reveal that a key germline-encoded contact between the T cell antigen receptor and a peptide underpins the immunodominance of dengue-virus-specific CD8⁺ T cell responses of weak affinity.

A new and unexpected role is identified for Srebps in controlling NK cell activity that is independent of their role in lipid biosynthesis.

By switching its partners, FoxP3 segregates into functional and non-functional transcriptional complexes.

The differentiation of follicular regulatory T cells can be limited by the cytokine IL-2, preventing the emergence of autoantibodies. This research identifies these cells as key regulators of the germinal center response.

The US National Institutes of Health convened a workshop on disease-promoting chronic inflammation to identify the challenges and needs in the development of clinically feasible strategies for monitoring a person's inflammation status before, during and after disease occurrence.

Recent decades have seen an alarming rise in the incidence of autoimmune disease. In a Perspective, Matarese and colleagues discuss the evidence showing that changes in diet and metabolic workload can account for, at least in part, rises in the frequency of autoimmune disease.

A two-amino-acid substitution in the transcription factor RORγt disrupts its effect in establishing the transcriptional program of T_H17 cells while leaving its function in the development of thymocytes and lymphoid-tissue–inducer cells largely intact.

T-bet⁺NKp46⁺ subsets of group 1 and group 3 innate lymphoid cells within the meninges initiate neuroinflammation in central nervous system (CNS)-demyelinating disease by regulating both the stability of pathogenic T-bet⁺ T cells and their access to the CNS.

Interferon-λ (IFN-λ) curbs neutrophil-mediated intestinal inflammation by diminishing the production of reactive oxygen species and subsequent oxidative stress. This regulatory process is unique to IFN-λ and is independent of interferon-induced transcription and translation programs.