T Cell Antagonism is Functionally Uncoupled from the 21- and 23-kDa Tyrosine-Phosphorylated TCR ζ Subunits
| Autor: | Nicolai S. C. van Oers, Pamela S. Ohashi, Lisa A. Pitcher |
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| Rok vydání: | 2003 |
| Předmět: |
Agonist
congenital hereditary and neonatal diseases and abnormalities medicine.drug_class Phenylalanine Receptors Antigen T-Cell alpha-beta T cell Protein subunit Amino Acid Motifs Immunology Receptors Antigen T-Cell Down-Regulation Mice Transgenic Biology Lymphocyte Activation Cell Line Mice T-Lymphocyte Subsets medicine Animals Immunology and Allergy Phosphorylation Tyrosine skin and connective tissue diseases Cell Membrane T-cell receptor Membrane Proteins Cell Differentiation Molecular biology Peptide Fragments Mice Inbred C57BL Molecular Weight Protein Subunits medicine.anatomical_structure Amino Acid Substitution Antagonism Intracellular |
| Zdroj: | The Journal of Immunology. 171:845-852 |
| ISSN: | 1550-6606 0022-1767 |
| Popis: | The functional effects of altered peptide ligands on T cells is proposed to involve differential intracellular signaling mediated by the 21- and 23-kDa tyrosine-phosphorylated derivatives of the TCR ζ subunit (p21 and p23). To understand the functional contribution of p21 and p23 to T cell development and T cell antagonism, we generated selected TCR ζ transgenic mice maintained on the P14 αβ TCR transgenic line such that p23 or both p21 and p23 were selectively eliminated. Importantly, one line (YF1,2) retains the constitutively tyrosine-phosphorylated p21 in the complete absence of inducible p23. We determined that T cell development was uncoupled from p21 and/or p23. Using a series of agonist, weak agonist, and antagonist peptides, we analyzed the role of each of the phosphorylated forms of TCR ζ on T cell activation and antagonism. In this study, we report that the proliferative responses of αβ P14 T cells to agonist peptides and the inhibition of proliferation resulting from antagonist peptide treatments was functionally uncoupled from p21 and/or p23. These results suggest that the mechanism of T cell antagonism is independent of the two phosphorylated TCR ζ derivatives. |
| Databáze: | OpenAIRE |
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