Issues

This Pillars of Immunology article is a commentary on “A new T-cell receptor gene located within the alpha locus and expressed early in T-cell differentiation,” a pivotal article written by Y.-H. Chien, M. Iwashima, K. B. Kaplan, J. F. Elliott, and M. M. Davis, and published in Nature, in 1987. https://www.nature.com/articles/327677a0.

• Severity of asthma in TLR4-SNP mice is dependent on the allergen system.

• TLR4-SNP mice have reduced allergic inflammation when using the OVA-LPS model.

• TLR4-SNP mice have enhanced allergic responses when using the HDM model.

• Lupus B cells present an elevated metabolism preceding the onset of autoimmunity.

• Except for GC B cells, glucose largely drives the metabolism of lupus B cells.

• Lupus and control B cells require glycolysis and glutaminolysis in TI responses.

• AAV-mediated CD1d gene delivery to CD1d knockout mouse fails to rescue iNKT cells.

• Reintroducing adipocyte CD1d induces massive expansion of adipose T cells.

• CD8⁺ T cells induced by adipocyte CD1d cause adipocyte NLRP3 inflammasome activation.

• Nr4a1 plays crucial roles in Treg cell differentiation in the presence of CNIs.

• Nr4a1 deficiency impairs the induction of T cell tolerance in the presence of CNIs.

• Most γδ recent thymic emigrants are immature.

• Some γδ T cells complete maturation in the thymus, and others complete maturation in the periphery.

• A population of γδ thymocytes is thymic resident.

• Novel computational script TRACE can detect gene conversion from across the genome.

• TRACE detects gene conversion donors from both intra- and interchromosomal sources.

• TRACE outputs correlate with germinal center B cell physiology.

• CD4⁺ and CD8⁺ T cells show high but distinct longitudinal responses in pH1N1 patients.

• Expression of immune checkpoints on CD4⁺ and CD8⁺ T cells changed after pH1N1 infection.

• LL-37 induces cell death in autophagy-dysfunctional endothelial cells.

• Under this condition, the intracellular degradation of LL-37 is disturbed.

• Inhibition of neutrophil PKR suppresses neutrophil adhesion and migration.

• Genetic silencing of PKR diminishes CaMKII activation and actin polymerization.

• PKR inhibition suppresses neutrophil recruitment in mouse inflammatory diseases.

• eCIRP is released through GSDMD pores independent of pyroptotic cell death.

• GSDMD and eCIRP interact with each other and colocalize at the cell membrane.

• Targeting GSDMD by a pharmacological approach inhibits eCIRP release in sepsis.

• CERKL mediates protection against viral infection via two distinct mechanisms.

• CERKL specifically stabilizes TBK1 by impeding the K48-linked polyubiquitination.

• CERKL decreases SVCV P protein though preventing K63-linked polyubiquitination.

• Diverse binding properties are revealed for seven nanobodies against C4b.

• Cryo-electron microscopy structures of C4b–nanobody complexes indicate nanobodies’ modes of action.

• Nanobodies have therapeutic potential and are useful for labeling studies.

• Somatic hypermutation in four J_H and four J_κ introns extends for approximately 1 kb.

• Intron DNA sequences and enhancers do not delimit the 3′ boundary of SHM.

• V regions are likely targeted for mutation by proximity to the promoter.

• NK cellular response is inhibited by ovarian cancer patient ascites.

• Ascites alters NK cell gene expression involved in activation and cytotoxicity.

• CA125, found in high concentrations in ascites, inhibits NK cell function.

• IL-27 signaling directly induces CCL5 production by mouse and human T cells.

• Stat3 and Stat1 bind to the CCL5 promoter in IL-27–stimulated CD8⁺ T cells.

• IL-27–induced CCL5 production enhances antitumor activity.

• A llama was immunized with Qa-1^b/Qdm, ligand for NKG2A, to construct a VHH library.

• A single-domain TCR-like Ab, EXX-1, specific for Qa-1^b/Qdm, was identified.

• EXX-1 selectively blocks the NKG2A/Qa-1^b axis to promote NK lysis of target cells.