Ontology highlight
ABSTRACT: Background
Allergy, the most common disease of immune dysregulation, has a substantial genetic component that is poorly understood. Although complete disruption of T-cell receptor (TCR) signaling causes profound immunodeficiency, little is known about the consequences of inherited genetic variants that cause partial quantitative decreases in particular TCR-signaling pathways, despite their potential to dysregulate immune responses and cause immunopathology.Objective
We sought to elucidate how an inherited decrease in TCR signaling through CARD11, a critical scaffold protein that signals to nuclear factor κB (NF-κB) transcription factors, results in spontaneous selective accumulation of large numbers of T(H)2 cells.Methods
"Unmodulated" mice carry a Card11 single nuc
SUBMITTER: Altin JA
PROVIDER: S-EPMC3189857 | biostudies-literature | 2011 May
REPOSITORIES: biostudies-literature