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In this Review, Pearce and colleagues discuss the metabolic adaptation of immune cells to various tissues and how functional adaptation compared with maladaptation within the niche can affect tissue homeostasis.
In this Review, Chavakis and colleagues discuss the mechanisms that govern the adaptation of hematopoietic progenitor cells to inflammation and its effects on the pathogenesis of human disease.
In this Review, Natoli and Ostuni discuss the mechanisms of adaptation and memory in immunity, with the aim of providing basic concepts that rationalize the properties and molecular bases of these essential processes.
Novel single-cell profiling technologies have delineated the cellular and molecular landscapes that dominate the joints in rheumatoid arthritis and the skin and kidneys in systemic lupus erythematosus, shedding light on potential pathogenic mechanisms.
Although the molecular basis of most disease-associated single-nucleotide polymorphisms has remained elusive, an HIV-1 viral load–associated polymorphism (rs1015164) has been identified that marks expression of a long non-coding RNA that regulates the co-receptor CCR5 and thereby influences infection of CD4+ T cells.
The cytokine IL-15 controls the homeostasis and activation of CD8+ T cells and natural killer cells. A new study reveals the deubiquitinase Otub1 to be a negative regulator of IL-15 signaling, with important consequences for autoimmunity and anti-cancer immunity.
Cachexia is a reversible feature of inflammatory states that can become maladaptive in many diseases. A new study reveals a role for type I interferons on CD8+ T cells in mediating cachexia during viral infection.
A novel feedback loop coordinated by germinal center–specific signaling via the kinase AKT activates negative regulators of upstream BCR signaling to attenuate responses to antigen stimulation.
Expression of the immunosuppressive cytokines IL-10 and IL-35 by tumor-infiltrating regulatory T cells drives exhaustion of intratumoral CD8+ T cells through a common pathway dependent on the transcription factor BLIMP-1.
The cytokine IL-17 augments metabolism in fibroblastic reticular cells in lymph nodes, which enhances their proliferation and survival to support B cell responses during autoimmunity.
The transcription factor PU.1 is not needed for the maintenance of neutrophil identity but is essential for the prevention of excessive tissue damage due to a prolonged immune response. PU.1 restrains the activation of neutrophils by antagonizing the AP-1 transcription factor JunB.
Comprehensive immunity requires that cells sense intracellular pathogens. In their Review, Shao and colleagues describe mechanisms for the recognition of intracellular lipopolysaccharide and its essential role in responses to Gram-negative bacteria.
The N6-methyladenosine (m6A) RNA-modification pathway affects numerous aspects of immune responses. A new study now demonstrates that m6A modification of transcripts encoding lysosomal proteases limits the efficiency of tumor-antigen cross-presentation.
The mechanisms by which the cytokine IFN-λ regulates adaptive immune responses are poorly understood. A new study now reveals a novel IFN-λ-mediated signal-transmission system that enhances immunity after infection of the mouse respiratory tract with influenza virus.
The skin and intestine are unique environments at the front line of the immune system. Powrie and colleagues review the distinctive adaptations acquired by regulatory T cells at these barrier surfaces.
The identification of T cells recognizing antigen has historically depended on live-cell imaging. Through the use of neural network–based image analysis, T cell–priming events can now be identified in fixed archival tissues.
Recent studies indicate that macrophages utilize NAD+-biosynthetic pathways to control inflammation and cell survival during the immune response and aging.
Inflammasomes have been reported to function in a wide variety of innate immune cells; however, their activity now seems to be more restricted than previously thought.
