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The relationship between atopic dermatitis and air pollution has been long debated but has now been connected via the aryl hydrocarbon receptor and its control of skin innervation and the consequent triggering of an itch-scratch response.
The deubiquitinase USP15 acts with the ubiquitin ligase TRIM25 to activate a type I interferon response and exacerbate microbial and autoimmune neuroinflammation.
Different cellular sources and signaling mechanisms mediate the effects of IL-6 on the generation of pathogenic TH17 helper T cells and the suppression of Foxp3+ regulatory T cells.
Altered signaling via the T cell antigen receptor (TCR) promotes an adipose-tissue-like phenotype in invariant natural killer cells (iNKT cells) during thymic development and causes selective enrichment for iNKT cells in adipose tissues.
A surprising molecular mechanism underlying signal integration and programmed proliferation in adaptive immunity has been identified: the cell-cycle regulator Myc enables a lymphocyte to add up the strength of signals it receives and time its response accordingly.
Notch signaling promotes the maintenance of lung-resident CD8+ memory T cells that are transcriptionally poised for rapid effector responses but have heightened expression of inhibitory receptors, suggestive of tight regulation.
Deficiency in the RASGRP1 guanine-nucleotide-exchange factor leads to a novel primary immunodeficiency with impaired activation and proliferation of T cells and B cells and defective killing by cytotoxic T cells and natural killer cells.
By taking advantage of an MR1 tetramer to accurately detect mucosal-associated invariant T (MAIT) cells in both mice and humans, researchers defined the thymic development of MAIT cells.
Microglia are important facilitators of glioma proliferation and invasion. An important component of this process seems to be glioma-mediated suppression of microglial activation via S-nitrosylation of microglial caspase-3.
A cohort of immunodeficient children lead near-normal lives after bone marrow transplantation, despite a profound deficiency of innate lymphoid cells (ILCs).
Epithelial cells of the gut are heavily glycosylated. Kiyono and colleagues review the evidence for the importance of this glycosylation to immunity, host–microbiome interactions and immunopathology.
New findings show that the NLRP3 inflammasome is inactivated by disassembly of the inflammasome mediated by the kinase PKA and that this regulation might be negated in NLRP3-gain-of-function diseases.
The Drosophila immune system distinguishes live, and potentially harmful, bacteria from harmless dead bacteria through the use of a splice variant of the receptor PGRP-LC.
CD1a on Langerhans cells in the epidermis is the lipid receptor for the plant-derived allergen urushiol and self lipids and is a key amplifier of inflammatory responses in urushiol-induced contact dermatitis as well as in psoriasis.
Follicular helper T cells (TFH cells) sequentially acquire the potential to secrete interleukin 21 (IL-21) and IL-4. The shift from secretion of IL-21 to that of IL-4 modifies the nature of the 'help' signals delivered by TFH cells to germinal center (GC) B cells.
In this Review, Chen and colleagues discuss recent advances in understanding of the cGAS–STING pathway, focusing on the regulatory mechanisms and roles of this pathway in heath and disease.
Membrane immunoglobulin E (IgE) on germinal-center-like B cells, without engagement of IgE, uses the CD19-PI3K-Akt-IRF4 axis and the BLNK-Jnk-p38 axis, with the former used for plasma-cell differentiation and the latter used for apoptotic death.
