| First Author | Sugie K | Year | 2004 |
| Journal | Proc Natl Acad Sci U S A | Volume | 101 |
| Issue | 41 | Pages | 14859-64 |
| PubMed ID | 15465914 | Mgi Jnum | J:93480 |
| Mgi Id | MGI:3057102 | Doi | 10.1073/pnas.0406168101 |
| Citation | Sugie K, et al. (2004) Activation of naive CD4 T cells by anti-CD3 reveals an important role for Fyn in Lck-mediated signaling. Proc Natl Acad Sci U S A 101(41):14859-64 |
| abstractText | Although there was no impairment in IL-2 secretion and proliferation of Fyn-deficient naive CD4 cells after stimulation with antigen and antigen-presenting cells, stimulation of these cells with anti-CD3 and anti-CD28 revealed profound defects. Crosslinking of purified wild-type naive CD4 cells with anti-CD3 activated Lck and initiated the signaling cascade downstream of Lck, including phosphorylation of ZAP-70, LAT, and PLC-gamma1; calcium flux; and dephosphorylation and nuclear translocation of the nuclear factor of activated T cells (NFAT)p. All of these signaling events were diminished severely in Fyn-deficient naive cells activated by CD3 crosslinking. Coaggregation of CD3 and CD4 reconstituted this Lck-dependent signaling pathway in Fyn(-/-) T cells. These results suggest that when signaling of naive T cells is restricted to the T cell antigen receptor, Fyn plays an essential role by positive regulation of Lck activity. |
