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The role of B7-1 and B7-2 costimulation for the generation of CTL responses in vivo.
Both dendritic cells and macrophages can stimulate naive CD8 T cells in vivo to proliferate, develop effector function, and differentiate into memory cells.
Leucine aminopeptidase is not essential for trimming peptides in the cytosol or generating epitopes for MHC class I antigen presentation.
CD40-CD40 ligand interaction between dendritic cells and CD8+ T cells is needed to stimulate maximal T cell responses in the absence of CD4+ T cell help.
Characterizing the specificity and cooperation of aminopeptidases in the cytosol and endoplasmic reticulum during MHC class I antigen presentation.
The IL-1-dependent sterile inflammatory response has a substantial caspase-1-independent component that requires cathepsin C.
Endoplasmic reticulum aminopeptidase 1 (ERAP1) trims MHC class I-presented peptides in vivo and plays an important role in immunodominance.
MyD88-dependent IL-1 receptor signaling is essential for gouty inflammation stimulated by monosodium urate crystals.
Analysis of the role of bleomycin hydrolase in antigen presentation and the generation of CD8 T cell responses.
CD40 on APCs is needed for optimal programming, maintenance, and recall of CD8+ T cell memory even in the absence of CD4+ T cell help.
Identification of the cellular sensor that stimulates the inflammatory response to sterile cell death.
Mice completely lacking immunoproteasomes show major changes in antigen presentation.
Altered peptidase and viral-specific T cell response in LMP2 mutant mice.
Microbiota signalling through MyD88 is necessary for a systemic neutrophilic inflammatory response.
Multiple Cathepsins Promote Pro-IL-1? Synthesis and NLRP3-Mediated IL-1? Activation.
The Combined Deficiency of Immunoproteasome Subunits Affects Both the Magnitude and Quality of Pathogen- and Genetic Vaccination-Induced CD8+ T Cell Responses to the Human Protozoan Parasite Trypanosoma cruzi.
Specialized proteasome subunits have an essential role in the thymic selection of CD8(+) T cells.
Frontline Science: Multiple cathepsins promote inflammasome-independent, particle-induced cell death during NLRP3-dependent IL-1? activation.
The GTPase Rab39a promotes phagosome maturation into MHC-I antigen-presenting compartments.
Immune Sensing of Cell Death through Recognition of Histone Sequences by C-Type Lectin-Receptor-2d Causes Inflammation and Tissue Injury.