Reviews & Analysis

The chromatin signature of genomic enhancers in CD4⁺ T cells distinguishes asthmatic patients from healthy subjects.

Cells of the T_H9 subset of helper T cells differentiated in the presence of interleukin 1β (IL-1β) produce large amounts of IL-9 and IL-21 in a manner dependent on the transcription factors STAT1 and IRF1 and exhibit potent anticancer effects.

The pathogenesis of inflammatory bowel disease is orchestrated by specific subsets of cytokine-secreting T cells. The interleukin 9–producing subset of helper T cells contributes to the pathogenesis of inflammatory bowel disease in part by disrupting intestinal barrier function and impairing tissue-repair mechanisms.

The transcription factors Foxp1 and Foxo1 inhibit the differentiation of follicular helper T cells. On the other hand, the E3 ligase Itch targets Foxo1 for degradation to promote such differentiation.

Migrating dendritic cells follow precise navigational chemokine gradients established by lymph node stromal cells through their asymmetric expression of the atypical chemokine receptor CCRL1.

The transcription factors TCF-1 and LEF-1 have diverse roles in differentiation into the CD4⁺ lineage through means both dependent on and independent of the transcription factor Th-POK.

The DNA-damage sensor Rad50 couples the sensing of cytosolic DNA to the innate immunological adaptor CARD9 to stimulate DNA-dependent activation of the transcription factor NF-κB. This facilitates DNA virus–stimulated production of the cytokine IL-1β.

The colonization of the colon with commensal microflora drives the induction and population expansion of regulatory T cells, an immunological adaption needed to prevent mucosal inflammation. The epigenetic modifier Uhrf1 acts as a key molecular mediator of such expansion and the establishment of a harmonious mucosal environment.

Natural killer (NK) cells are innate lymphocytes that exhibit many features of adaptive immunity, such as long-lived memory. This can now be extended to the transcriptional circuits that control the proliferation of NK cells and lymphocytes.

The receptor CD96 inhibits cytokine production by natural killer cells in mice and antagonizes activation mediated by the receptor CD226.

Cytokines and other environmental cues influence polarization of CD4⁺ helper T cells, but the signaling pathways that are involved are less clear. Recent findings show that signaling via an mTORC2-SGK1 kinase axis regulates T_H1–T_H2 cell-fate polarization.

CTLA-4 is a potent inhibitor of T cell population expansion. The PIX-GIT2-PAK2 complex is recruited to the cytoplasmic domain of CTLA-4 via the kinase PKC-η, which suggests a previously unrecognized aspect of signal transduction via CTLA-4 in immunoregulation.

Although it is generally considered a proinflammatory cytokine, interleukin 6 (IL-6) has anti-inflammatory effects in macrophages by sensitizing them to IL-4 through upregulation of the IL-4 receptor.

Functional coupling of receptors for immunoglobulin G (FcγRI) and interferon-γ (IFN-γR) generates a context-dependent signaling pathway in macrophages.

The PYRIN domain–only protein POP3 sets limits for activation of the AIM2 inflammasome after cytosolic double-stranded DNA is sensed.

The activation of dendritic cells by Toll-like receptors leads to a rapid enhancement in glycolysis. Glucose is metabolized to pyruvate and from there to citrate in the mitochondria, which leads ultimately to membrane biosynthesis in the endoplasmic reticulum and Golgi to support the activation of dendritic cells.

Innate lymphoid cells, marginal reticular cells and B cell–helper neutrophils interact to promote antibody secretion by B cells in the marginal zone of the spleen in humans and mice.

Hyperactivity of a branch of the unfolded protein response in CD8α⁺ dendritic cells degrades endoplasmic reticulum–associated mRNAs, which leads to a defect in the cross-presentation of dead cell–derived antigens.

Naive T cells differentiate into memory subsets upon exposure to their cognate foreign antigen. However, before such encounters, some naive T cells are 'imprinted' through their interactions with self targets.

Phosphorylation of the adhesion molecule VE-cadherin at tyrosine residues modulates the opening of endothelial junctions during inflammatory reactions. The replacement of two distinct residues in VE-cadherin shows that Tyr685 regulates vascular permeability and Tyr731 regulates leukocyte diapedesis in vivo.