학술논문

Ribp, a Novel Rlk/Txk- and Itk-Binding Adaptor Protein That Regulates T Cell Activation
Document Type
article
Source
Journal of Experimental Medicine. 190(11)
Subject
Hematology
Rare Diseases
Cancer
Aetiology
Underpinning research
1.1 Normal biological development and functioning
2.1 Biological and endogenous factors
Inflammatory and immune system
Adaptor Proteins
Signal Transducing
Amino Acid Sequence
Animals
Carrier Proteins
Cell Line
Cells
Cultured
Chromosome Mapping
Cloning
Molecular
Crosses
Genetic
Gene Library
Humans
Interleukin-2
Killer Cells
Natural
Lymphocyte Activation
Lymphoma
T-Cell
Mice
Mice
Inbred Strains
Mice
Knockout
Molecular Sequence Data
Muridae
Protein-Tyrosine Kinases
Recombinant Proteins
Sequence Alignment
Sequence Homology
Amino Acid
T-Lymphocytes
Transfection
Tumor Cells
Cultured
T cell activation
signal transduction
adaptor protein
Tec tyrosine kinases
T helper type 1/T helper type 2 cells
Medical and Health Sciences
Immunology
Language
Abstract
A novel T cell-specific adaptor protein, RIBP, was identified based on its ability to bind Rlk/Txk in a yeast two-hybrid screen of a mouse T cell lymphoma library. RIBP was also found to interact with a related member of the Tec family of tyrosine kinases, Itk. Expression of RIBP is restricted to T and natural killer cells and is upregulated substantially after T cell activation. RIBP-disrupted knockout mice displayed apparently normal T cell development. However, proliferation of RIBP-deficient T cells in response to T cell receptor (TCR)-mediated activation was significantly impaired. Furthermore, these activated T cells were defective in the production of interleukin (IL)-2 and interferon gamma, but not IL-4. These data suggest that RIBP plays an important role in TCR-mediated signal transduction pathways and that its binding to Itk and Rlk/Txk may regulate T cell differentiation.