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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.
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.
Adenosine produced by apoptotic regulatory T cells (Treg cells) has a more important immunosuppressive role in the tumor microenvironment than that of live Treg 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.
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.
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.
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.
A two-amino-acid substitution in the transcription factor RORγt disrupts its effect in establishing the transcriptional program of TH17 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.
Caveolin-1 has a critical role in orchestrating the membrane organization of B cells. In its absence, signaling via the B cell antigen receptor and B cell tolerance are impaired, which results in autoimmunity.
Poor glycolysis and increased fatty-acid synthesis feed the locomotion machinery in T cells from people with rheumatoid arthritis and allow these cells to enter the synovium and propagate joint inflammation and destruction.
The ability to expand and contract populations of myeloid and lymphoid cells during emergency hematopoiesis helps shape the immune response. The expression of intracellular and soluble forms of osteopontin regulates apoptosis thresholds differently in myeloid cells and lymphoid cells to counter infection.
The histone lysine methyltransferase MLL4 primes the locus encoding the transcription factor Foxp3 for transcriptional activation in thymus-derived and inducible regulatory T cells.
The cytokine TGF-β allows tumors to evade the immune system by converting conventional natural killer cells into type 1 innate lymphoid cells devoid of cytotoxic function.