PILLARS OF IMMUNOLOGY
This Pillars of Immunology article is a commentary on “Toll-like receptor 9-mediated recognition of herpes simplex virus-2 by plasmacytoid dendritic cells,” a pivotal article written by J. Lund, A. Sato, S. Akira, R. Medzhitov, and A. Iwasaki, and published in the Journal of Experimental Medicine, in 2003. https://doi.org/10.1084/jem.20030162.
Cutting Edge: Neutrophil Complement Receptor Signaling Is Required for BAFF-Dependent Humoral Responses in Mice
Granulocyte-expressed C3aR1 and C5aR1 drive T-independent humoral responses.
The effects are mediated through upregulation of neutrophil BAFF.
Analogous mechanisms are required for optimal mucosal IgA production.
CLINICAL AND HUMAN IMMUNOLOGY
Follicle-Stimulating Hormone Provokes Macrophages to Secrete IL-1β Contributing to Atherosclerosis Progression
FSH could induce the inflammatory differentiation of macrophages.
FSH remarkably promoted the expression and secretion of IL-1β in macrophages.
The chemotactic migratory capacity of macrophages was promoted by FSH.
CD8+CXCR5+ T cells are elevated in HIV+ MACS participants.
Activated CD8+CXCR5+ T cells induce PD-L1+ and PD-L1+IgG+ B cells.
CD8+CXCR5+ T cells significantly and positively correlate with PD-L1+ B cells.
IMMUNE SYSTEM DEVELOPMENT
Diversity in Cortical Thymic Epithelial Cells Occurs through Loss of a Foxn1-Dependent Gene Signature Driven by Stage-Specific Thymocyte Cross-Talk
cTECs undergo progressive changes during postnatal life caused by loss of Foxn1.
Foxn1− cTECs remain within the cortex but lack cTEC signature genes.
Foxn1− cTECs show an impaired ability to influence developing thymocytes.
IMMUNOTHERAPY AND VACCINES
Synergistic Protection against Secondary Pneumococcal Infection by Human Monoclonal Antibodies Targeting Distinct Epitopes
The mAb PhtD3 mechanism of protection is mediated by macrophages and complement system.
The mAbs PhtD3 and PhtD7 produce robust protection in an influenza coinfection model.
INNATE IMMUNITY AND INFLAMMATION
Regulation of Synovial γδ T Cell Ligand Expression by Mitochondrial Reactive Oxygen Species and Gasdermin-D
Human synovial TCR-γδ ligand is induced on monocytes by TLR stimuli.
Ligand surface expression is dependent on gasdermin-D and is redox sensitive.
Ligand expression intracellularly colocalizes with mitochondria.
INFECTIOUS DISEASE AND HOST RESPONSE
Spring Viremia of Carp Virus N Protein Negatively Regulates IFN Induction through Autophagy-Lysosome–Dependent Degradation of STING
SVCV N protein negatively regulates cellular IFN production.
SVCV N protein degrades STING in an autophagy-lysosome–dependent manner.
Beclin1 is essential for N protein–mediated autophagic degradation of STING.
Longitudinal Immune Profiling Highlights CD4+ T Cell Exhaustion Correlated with Liver Fibrosis in Schistosoma japonicum Infection
Single-cell RNA sequencing revealed the cellular components after S. japonicum infection.
B and myeloid cells showed inhibitory interactions with exhausted CD4+ T cells.
Exhausted CD4+ T cells promoted collagen expression in HSCs via IL-4 secretion.
MOLECULAR AND STRUCTURAL IMMUNOLOGY
Mass spectrometry analyses show that chicken MHCY class I molecules bind lysophospholipids.
MHCY class I molecules differing significantly in sequence bind the same ligands.
Residues mostly away from the binding groove define MHCY class I polymorphism.
Structural similarity is highly correlated with peptide binding specificity.
A comprehensive HLA supertype classification method is presented.
Improved breadth, accuracy, flexibility, and stability relative to previous methods are shown.
On the cover: Structural representation of a peptide–HLA complex (Protein Data Bank ID: 3TO2) showing six characteristic binding pockets (A–F) along the binding groove. The peptide is shown in rainbow color with the N terminus in purple and the C terminus in orange. Pockets are colored the same as the closest peptide residue. Shen, Y., J. M. Parks, and J. C. Smith. 2023. HLA class I supertype classification based on structural similarity. J. Immunol. 210: 103–114.
- PDF Icon PDF LinkFront Matter
- PDF Icon PDF LinkTable of Contents
- PDF Icon PDF LinkBack Matter
- PDF Icon PDF LinkEditorial Board