Reviews & Analysis

ThPOK, the critical transcription factor for differentiation of the helper T cell lineage in the thymus, continues to function as a gatekeeper to maintain helper T cell identity by repressing the transcription factor Runx3 in mature T cells.

Transcriptional profiling of endothelial cells from diverse secondary lymphoid organs reveals distinctions that underlie their functional specification.

The transcriptional regulator Bcl-6 represses aerobic glycolysis in CD8⁺ and CD4⁺ type 1 helper T cells.

The ER stress response is a well-characterized process aimed at restoring ER function. Lambrecht et al. explore how ER stress can also intersect with the innate and adaptive immune response at multiple levels.

A ligand and G protein–coupled receptor activate antimicrobial gene expression in the Caenorhabditis elegans epidermis, in response to wounding and to infection with a fungal pathogen.

AP4, a transcription factor induced by the functionally related transcription factor c-Myc, maintains the cellular metabolic program for the sustained activation and population expansion of CD8⁺ T cells after the dynamic loss of c-Myc expression.

The unfolded protein response produces modified endogenous RNA substrates for host cytosolic sensors of RNA, which may lead to production of the interferons IFN-α and IFN-β. The accrual of modified RNA is prevented by an RNA nuclease.

TCR ligation activates multiple downstream pathways that lead to myriad functional outputs. Malissen and colleagues discuss how unbiased mass spectrometry using signaling hub 'bait' molecules, such as Lat, provides new insight into TCR signaling cascades.

How agonist peptides initiate the T cell antigen receptor (TCR) signaling cascade is widely debated. Weiss and Chakraborty discuss current models of the proximal signaling events that ensue upon recognition of agonist peptide–MHC complexes by TCRs.

Thymocytes and mature T cells are exposed to a broad range of self-peptides of varying reactivity with TCRs. Hogquist and Jameson discuss how differences in self-reactivity and TCR signal strength dictate subsequent cell fates.

TCR engagement triggers activation of downstream kinases. Navarro and Cantrell discuss how the network of serine/threonine kinases instruct T cell metabolism to participate in immune responses.

Infection with an RNA virus induces the interferons IFN-β and IFN-λ via the adaptor MAVS located in mitochondria, while peroxisomal MAVS selectively activates an IFN-λ response.

Inflammasome-driven inflammation extends into the extracellular space and to neighboring cells through the passive release of specks consisting of the adaptor ASC; this perpetuates the innate immune response and adds a dimension beyond interleukin 1 to autoinflammation.

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.