Toyooka Lab

Translational Research for Autism & Parkinson's Disease

CD5 Costimulation Up-Regulates the Signaling to Extracellular Signal-Regulated Kinase Activation in CD4+CD8+ Thymocytes and Supports Their Differentiation to the CD4 Lineage1


Journal article


Xuyu Zhou, Y. Yashiro‐Ohtani, K. Toyo-oka, C. Park, X. Tai, T. Hamaoka, H. Fujiwara
The Journal of Immunology, 2000

Semantic Scholar DOI PubMed
Cite

Cite

APA   Click to copy
Zhou, X., Yashiro‐Ohtani, Y., Toyo-oka, K., Park, C., Tai, X., Hamaoka, T., & Fujiwara, H. (2000). CD5 Costimulation Up-Regulates the Signaling to Extracellular Signal-Regulated Kinase Activation in CD4+CD8+ Thymocytes and Supports Their Differentiation to the CD4 Lineage1. The Journal of Immunology.


Chicago/Turabian   Click to copy
Zhou, Xuyu, Y. Yashiro‐Ohtani, K. Toyo-oka, C. Park, X. Tai, T. Hamaoka, and H. Fujiwara. “CD5 Costimulation Up-Regulates the Signaling to Extracellular Signal-Regulated Kinase Activation in CD4+CD8+ Thymocytes and Supports Their Differentiation to the CD4 Lineage1.” The Journal of Immunology (2000).


MLA   Click to copy
Zhou, Xuyu, et al. “CD5 Costimulation Up-Regulates the Signaling to Extracellular Signal-Regulated Kinase Activation in CD4+CD8+ Thymocytes and Supports Their Differentiation to the CD4 Lineage1.” The Journal of Immunology, 2000.


BibTeX   Click to copy

@article{xuyu2000a,
  title = {CD5 Costimulation Up-Regulates the Signaling to Extracellular Signal-Regulated Kinase Activation in CD4+CD8+ Thymocytes and Supports Their Differentiation to the CD4 Lineage1},
  year = {2000},
  journal = {The Journal of Immunology},
  author = {Zhou, Xuyu and Yashiro‐Ohtani, Y. and Toyo-oka, K. and Park, C. and Tai, X. and Hamaoka, T. and Fujiwara, H.}
}

Abstract

CD5 positively costimulates TCR-stimulated mature T cells, whereas this molecule has been suggested to negatively regulate the activation of TCR-triggered thymocytes. We investigated the effect of CD5 costimulation on the differentiation of CD4+CD8+ thymocytes. Coligation of thymocytes with anti-CD3 and anti-CD5 induced enhanced tyrosine phosphorylation of LAT (linker for activation of T cells) and phospholipase C-γ (PLC-γ) compared with ligation with anti-CD3 alone. Despite increased phosphorylation of PLC-γ, this treatment down-regulated Ca2+ influx. In contrast, the phosphorylation of LAT and enhanced association with Grb2 led to activation of extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase. When CD3 and CD5 on CD4+CD8+ thymocytes in culture were coligated, they lost CD8, down-regulated CD4 expression, and induced CD69 expression, yielding a CD4+(dull)CD8−CD69+ population. An ERK inhibitor, PD98059, inhibited the generation of this population. The reduction of generation of CD4+CD8− cells resulted from decreased survival of these differentiating thymocytes. Consistent with this, PD98059 inhibited the anti-CD3/CD5-mediated Bcl-2 induction. These results indicate that CD5 down-regulates a branch of TCR signaling, whereas this molecule functions to support the differentiation of CD4+CD8+ thymocytes by up-regulating another branch of TCR signaling that leads to ERK activation.