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Cited by 29

The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.

TCR/CD3 Down-Modulation and ζ Degradation Are Regulated by ZAP-70

Dumont, Céline, Blanchard, Nicolas, Di Bartolo, Vincenzo, Lezot, Nathalie, Dufour, Evelyne, Jauliac, Sébastien, Hivroz, Claire·2002·The Journal of Immunology
DOI 10.4049/jimmunol.169.4.1705
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Abstract

TCR down-modulation following binding to MHC/peptide complexes is considered to be instrumental for T cell activation because it allows serial triggering of receptors and the desensitization of stimulated cells. We studied CD3/TCR down-modulation and ζ degradation in T cells from two ZAP-70-immunodeficient patients. We show that, at high occupancy of the TCR, down-modulation of the CD3/TCR is comparable whether T cells express or do not express ZAP-70. However, if TCR occupancy was low, we found that CD3/TCR was down-regulated to a lesser extent in ZAP-70-negative than in ZAP-70-positive T cells. We studied CD3/TCR down-modulation in P116 (a ZAP-70-negative Jurkat cell-derived clone) and in P116 transfected with genes encoding the wild-type or a kinase-dead form of ZAP-70. Down-modulation of the TCR at high occupancy did not require ZAP-70, whereas at low TCR occupancy down-modulation was markedly reduced in the absence of ZAP-70 and in cells expressing a dead kinase mutant of ZAP-70. Thus, the presence of ZAP-70 alone is not sufficient for down-modulation; the kinase activity of this molecule is also required. The degradation of ζ induced by TCR triggering is also severely impaired in T cells from ZAP-70-deficient patients, P116 cells, and P116 cells expressing a kinase-dead form of ZAP-70. This defect in TCR-induced ζ degradation is observed at low and high levels of TCR occupancy. Our results identify ZAP-70, a tyrosine kinase known to be crucial for T cell activation, as a key player in TCR down-modulation and ζ degradation.

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Citations

Cites

Research works printed but not linked: 49

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Metadata

Authors
Dumont, C., Blanchard, N., Di Bartolo, V., Lezot, N., Dufour, E., Jauliac, S., & Hivroz, C.
Affiliations
  • Institut National de la Santé et de la Recherche Médicale, Unité 520, Institut Curie , Paris ,
  • Molecular Immunology Unit, Institut Pasteur , Paris ,
  • Department of Pathology, Beth Israel Deaconess Medical Center , Boston, MA 02215
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2002-08
Volume
169
Issue
4
Pages
1705-1712
ISSN
  • 0022-1767
  • 1550-6606
DOI
10.4049/jimmunol.169.4.1705
Cited by
29
References
49
Language
en
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)

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