title: Altered T-cell receptor signaling in the pathogenesis of allergic disease.
abstract: Mounting evidence from animal models has demonstrated that alterations in T-cell receptor (TCR) signaling alone can lead to dramatically skewed differentiation of naive T cells into T(H)2 cells, to T(H)2 effector functions, and to T(H)2-related diseases. There is significant potential relevance of these observations to human disease. Specifically, a number of immunodeficiencies associated with atopic disease might have atopy as a manifestation because of aberrant TCR signaling. It is therefore important to attempt to identify a role for defects in TCR signaling in the pathogenesis of common atopic diseases.
authors.affiliation: Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA.
authors.forename: Shrimati
authors.initials: S
authors.lastname: Datta
authors.forename: Joshua D
authors.initials: JD
authors.lastname: Milner
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000502:physiology; D000818:Animals; D050990:GATA3 Transcription Factor / Q000502:physiology; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology* / Q000276:immunology; D016130:Immunophenotyping; D008565:Membrane Proteins / Q000502:physiology; D011948:Receptors, Antigen, T-Cell / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D050378:T-Lymphocytes, Regulatory / Q000502:physiology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D050990:GATA3 Transcription Factor; C494749:GATA3 protein, human; C110810:LAT protein, human; D008565:Membrane Proteins; D011948:Receptors, Antigen, T-Cell