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The accumulation of intestinal Foxp3+ regulatory T cells (Treg cells) in response to the microbiota is tightly regulated. Epithelial apoptosis inhibits the production of tolerogenic interferon-β by myeloid cells and thereby reduces the frequency of Treg cells and lowers the threshold for inflammatory responses.
SHARPIN acts independently of the ubiquitin-assembly complex LUBAC to attenuate proximal signaling downstream of TCRs by inhibiting the interaction of Zap70 with the TCRζ chain through Lys63 (K63)-linked polyubiquitination. SHARPIN deficiency enhanced TCR signaling and impaired the development and function of Treg cells.
The NLRP3 inflammasome has broad biomedical relevance, but its activation mechanisms are incompletely understood. NEK7, a kinase that regulates microtubules during mitosis, is identified as a critical and selective upstream regulator of NLRP3 inflammasome activation.
The production of interleukin 12 (IL-12) and IL-23 in dendritic cells is strictly regulated via epigenetic silencing. This transcriptional repression is overcome with the help of the deubiquitinase Trabid and has functional implications in a mouse model of multiple sclerosis.
An important new function for the phosphatase PTEN in regulating interferon responses to viral infection has been delineated. This finding could help explain the remarkable cancer selectivity of many oncolytic viruses.
Thymic selection shapes the repertoire of potentially autoreactive thymocytes that are allowed to mature. The expression pattern of self antigen seen by thymocytes determines the number and functional ability of autoreactive T cells.
Viral infection of the mucosa induces a strong host innate immune response involving type I interferons and interferon-stimulated genes. New findings show that mechanical or pathogen-induced disruption of the mucus itself can also trigger 'hyper-early' innate responses independent of type I interferons and major sensing pathways of the innate immune system.
Systems immunology identifies molecular and cellular signatures associated with adverse clinical events and antibody response to a vaccine against H1N1 influenza virus.
Arteries are colonized by macrophages of multiple origins, derived prenatally from the yolk sac and during an early postnatal wave from the bone marrow. During sepsis, blood monocyte-derived macrophages transiently contribute to, but do not replace, resident arterial macrophages that largely self-renew in situ.
Low availability of glucose in tumors negatively affects the activity of tumor-infiltrating T cells. Loss of T cell function under these conditions is mediated by the microRNAs miR-101 and miR-26a, which target expression of the methytransferase EZH2 and thereby diminish the expression of anti-tumor cytokines.
Understanding cytotoxic T cells has been a major focus of immunology research for decades. Proteomic profiling of these cells now brings them into unprecedented and revealing focus.
Immune responses are characterized by the concerted actions of both effector mechanisms and regulatory mechanisms. Signaling via the transcription factor STAT1 downstream of receptors for interferons and interleukin 27 (IL-27) can suppress type 2 immune responses induced by group 2 innate lymphoid cells (ILCs).
Small, soluble, ubiquitous ligands are difficult to visualize. Schwab and colleagues have created a functional receptor reporter that gauges the in vivo concentration, location and biological action of sphingolipids.
The transcription factor Nr4a1 can negatively regulate norepinephrine production in the context of neuroinflammation and thereby prevent the ensuing neuroinflammatory cascade in a mouse model of experimental autoimmune encephalomyelitis.
Mitochondria can contribute to an increase in the amount of phagosomal reactive oxygen species and thereby promote the effective killing of bacteria. Study of mice deficient in Mst1 and Mst2 reveals a role for these kinases in recruiting mitochondria to phagosomes.
Docking of T cell antigen receptors (TCRs) engaging complexes of peptide and major histocompatibility complex has shown the same diagonal orientation and polarity. A new study demonstrating that TCRs from regulatory T cells bind with reversed polarity challenges this dogma.
The TH17 subset of helper T cells drives emphysema in smokers, but how these cells are elicited remains unknown. A study now links the microRNA miR-22 and the histone deacetylase HDAC4 to regulation of the activation of antigen-presenting cells after exposure to smoke.
Paradoxically, radiotherapy can reinforce immunosuppressive pathways that undermine anticancer immunosurveillance and treatment efficacy. Irradiation induces Langerhans cells to migrate from the skin to lymph nodes, where they stimulate regulatory T cells.
Immature B lymphocytes and T lymphocytes assemble antigen receptor–encoding genes in lineage- and developmental stage–specific fashion. New findings show that pre-B cells use specialized locus-specific epigenetic mechanisms to promote recombination of the locus encoding the immunoglobulin κ-chain (Igk) and κ-chain+ B cell development.
