TY - JOUR
T1 - T cell receptor-mediated activation of CD4+CD44hi T cells bypasses Bcl10
T2 - An implication of differential NF-κB dependence of naïve and memory T cells during T cell receptor-mediated responses
AU - Zeng, Hu
AU - Chen, Yuhong
AU - Yu, Mei
AU - Xue, Liquan
AU - Gao, Xiang
AU - Morris, Stephan W.
AU - Wang, Demin
AU - Wen, Renren
PY - 2008/9/5
Y1 - 2008/9/5
N2 - Previous studies have demonstrated that Bcl10 (B-cell leukemia/lymphoma 10) is essential for T cell receptor-mediated NF-κB activation and subsequent proliferation and interleukin 2 (IL2) production. However, here we demonstrate that, contrary to expectations, Bcl10 is differentially required for T cell activation, including for both proliferation and cytokine production. When CD4+ and CD8+ T cells were divided based on expression levels of CD44, which distinguishes naïve cells (CD44lo) versus those that are antigen-experienced (CD44hi), IL2 production by and proliferation of CD4+CD44lo naïve cells and both subpopulations of CD8+ T cells were clearly Bcl10-dependent, whereas these same functional properties of CD4+CD44hi T cells occurred largely independent of Bcl10. As with the other subpopulations of T cells, CD4+CD44hi T cells did not activate the NF-κB pathway in the absence of Bcl10; nevertheless, these CD4+CD44 hi antigen-experienced T cells efficiently secreted IL2 after T cell receptor stimulation. Strikingly, therefore, T cell receptor-mediated IL2 production in these cells is NF-κB-independent. Our studies suggest that antigen-experienced CD4+ T cells differ from their naïve counterparts and from CD8+ T cells in their ability to achieve activation independent of the Bcl10/NF-κB pathway.
AB - Previous studies have demonstrated that Bcl10 (B-cell leukemia/lymphoma 10) is essential for T cell receptor-mediated NF-κB activation and subsequent proliferation and interleukin 2 (IL2) production. However, here we demonstrate that, contrary to expectations, Bcl10 is differentially required for T cell activation, including for both proliferation and cytokine production. When CD4+ and CD8+ T cells were divided based on expression levels of CD44, which distinguishes naïve cells (CD44lo) versus those that are antigen-experienced (CD44hi), IL2 production by and proliferation of CD4+CD44lo naïve cells and both subpopulations of CD8+ T cells were clearly Bcl10-dependent, whereas these same functional properties of CD4+CD44hi T cells occurred largely independent of Bcl10. As with the other subpopulations of T cells, CD4+CD44hi T cells did not activate the NF-κB pathway in the absence of Bcl10; nevertheless, these CD4+CD44 hi antigen-experienced T cells efficiently secreted IL2 after T cell receptor stimulation. Strikingly, therefore, T cell receptor-mediated IL2 production in these cells is NF-κB-independent. Our studies suggest that antigen-experienced CD4+ T cells differ from their naïve counterparts and from CD8+ T cells in their ability to achieve activation independent of the Bcl10/NF-κB pathway.
UR - http://www.scopus.com/inward/record.url?scp=54049097968&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=54049097968&partnerID=8YFLogxK
U2 - 10.1074/jbc.M802344200
DO - 10.1074/jbc.M802344200
M3 - Article
C2 - 18583339
AN - SCOPUS:54049097968
SN - 0021-9258
VL - 283
SP - 24392
EP - 24399
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 36
ER -