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Tumors can evade immune system–mediated destruction despite expressing antigenic neoepitopes. Gajewski, Schreiber and Fu discuss how the tumor microenvironment harnesses innate and adaptive immune cell regulatory processes to promote tumor survival.
Macrophages populate tissues under homeostatic conditions. Taylor and colleagues discuss the heterogeneity of tissue macrophage populations, and how they contribute to tissue function and immune surveillance.
Regulatory T (Treg) cells modulate immune cell responses. Mathis and colleagues review the specialized roles played by tissue-specific Treg cells and reveal new functions that can be attributed to distinct Treg cell subsets.
The liver is important in mediating immunity to blood-borne infections. Jenne and Kubes review the liver as an immune organ and discuss the roles of liver-resident cells and their interactions with circulating immune cells.
In the absence of the SCARF1 scavenger system in mice, the load of 'dangerous' molecules can increase, inducing features of lupus in a sex-dependent process. These findings highlight the interplay of death and sex in the generation of autoimmunity.
A unique complex of the interferon receptor IFNAR1 and interferon-β (IFN-β) has been identified that signals independently of IFNAR2 and induces a distinct set of interferon-inducible genes and downstream IFN-β-specific functional responses.
Small phosphorylated prenyl metabolites are potent activators of γδ T cells in human peripheral blood, but the molecular mechanism underlying their antigenic potency has remained a mystery. New data identify BTN3A1 as a novel antigen-presentation molecule for both microbial and host-derived phosphorylated antigens.
CD11b+ dendritic cells (DCs) represent a subset of classical DCs that require signaling via the receptor Notch2 and lymphotoxin-β receptor and act as obligate source of interleukin 23 for protection against Citrobacter rodentium.
Sterols and oxysterol derivatives of cholesterol regulate diverse cellular processes. Nathanael Spann and Christopher Glass review the emerging data indicating that these endogenous compounds also serve key roles in almost all aspects of immunological function.
Resistance to infection of the skin with Staphylococcus aureus depends on early production of interleukin 1β (IL-1β) and IL-17A by skin-resident cells. However, several members of the IL-20 subfamily of cytokines (IL-19, IL-20 and IL-24) can inhibit the local generation of those two cytokines.
Platelets and phagocytes engage in bidirectional interaction in innate immunity and inflammation. Kupffer cell–platelet cooperation results in the rapid encasement of blood-borne bacteria and host protection.
Studies have linked the NLRP3 inflammasome pathway to the elaboration of sterile inflammation. CD36 serves a dual role by priming transcription of the gene encoding interleukin 1β (IL-1β) and inducing assembly of the NLRP3 inflammasome complex, which leads to the release of active IL-1β.
The generation of T cell–dependent humoral immunity is regulated by the miR-17∼92 cluster of microRNAs through their influence on the differentiation and function of follicular helper T cells.
Members of the SOCS (suppressor of cytokine signaling) family negatively regulate STAT transcription factors. The SOCS family member CIS is now shown to negatively regulate differentiation into the TH2 and TH9 subsets of helper T cells through negative regulation of STAT3, STAT5 and STAT6.
A third population of human T lymphocytes that express αβ T cell antigen receptors with restricted α-chain diversity has been identified. These cells recognize the lipid glucose monomycolate from Mycobacterium tuberculosis presented by CD1b.
The glycoprotein CD52 is an important target for clinical antibodies, but its receptor and function have remained a mystery. However, it now seems that CD52 may be released in soluble form by a subpopulation of human T cells and may thereby exert an as-yet-unrecognized regulatory function via the inhibitory molecule Siglec-10.
