Browse the search results

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

An interpretable machine learning approach can recapitulate the molecular features associated to immune protein-protein binding and leverage them for the prediction of immune response specificity.

Systems analysis of antibody repertoires reveals that strong humoral responses lead to extensive B-cell overlap across multiple lymphoid organs, indicating physiological axes of B-cell migration and a direct correlation with antigen specificity.

The tissue environment shapes the lipid recognition capacity of natural killer T cells.

The T cell repertoire can display immunodominance to an epitope as a result of optimal positive selection in the thymus by one self-peptide/MHC ligand.

By using immune cells called dendritic cells to deliver drugs, it is possible to target and kill specific members of another class of immune cell, known as T cells, and to prevent these cells from attacking the body's own tissues in cases of autoimmune disease.

Distance-based TCR analysis enables grouping of biochemically similar clonotypes into meta-clonotypes that have increased publicity, and therefore statistical power, for population-level detection of antigen-specific T cells in infection and vaccination.

Human macrophages infected with Mycobacterium tuberculosis present peptides derived from substrates of type VII secretion systems on MHC class I via a pathway dependent on the ESX-1 secretion system and independent of antigen processing by the proteasome and cathepsins.

Important nonlinear links between infection, inflammation, and disease severity were revealed using experimentally validated mathematical models.

Osteoarthritis pathogenesis is driven by IgE-mediated mast cell activation.