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MHC class II-mediated self-antigen presentation by lymph node stromal cells controls regulatory T cell homeostasis, thus safeguarding immune tolerance.

Immune stimulation from the microbiota prevents neurological damage associated with viral infection of the central nervous system.

In vivo modeling of neoantigen-restricted heterogeneity shows that clonal expression of neoantigens enhances anti-tumor T cell responses by increasing the stimulatory capacity of dendritic cells in the lymph node.

Direct control of ligand binding half-life with light shows that lifetime strongly affects T cell signaling.

All-atom molecular dynamics simulations of an αβ T-cell receptor complexed with the major histocompatibility complex molecule presenting wild-type or mutant antigenic peptides reveal how it uses conserved framework motion to discriminate antigens by leveraging physiological force applied during immune surveillance.

Tumors escape killing by the immune system through generating transient spatial cell-in-cell structures that are impenetrable to cytotoxic compounds including lytic granules and chemotherapy.

The AlphaFold protein structure prediction network can be specialized for T cell receptor docking, leading to improved models of ternary complexes and some ability to discriminate correct from incorrect peptide epitopes.

Yeast surface-displayed libraries, when coupled with pooled oligonucleotide synthesis and next-generation sequencing, can be used as a platform to assess binding of whole viral proteomes to class II major histocompatibility complex proteins.

Adjuvants, MPLA and CpG especially, modulate the peptide repertoires presented on the surface of APCs, preferring the presentation of low-affinity exogenous peptides rather than high-affinity peptides.

A single point mutation in a Ras activator leads to aberrant constitutive mTOR signaling in peripheral T cells that consequently accumulate as abnormal T helper cells and stimulate the production of autoantibodies by B cells.