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A critical role for direct TLR2-MyD88 signaling in CD8 T-cell clonal expansion and memory formation following vaccinia viral infection.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Quigley, Michael Martínez, Jénnifer Huang, Xiaopei Yang, Yiping |
| Copyright Year | 2009 |
| Abstract | Recent advances have suggested a crucial role of the innate immunity in shaping adaptive immune responses. How activation of innate immunity promotes adaptive T-cell responses to pathogens in vivo is not fully understood. It has been thought that Toll-like receptor (TLR)-mediated control of adaptive T-cell responses is mainly achieved by the engagement of TLRs on antigen-presenting cells to promote their maturation and function. In this study, we showed that direct TLR2-myeloid differentiating factor 88 (MyD88) signaling in CD8 T cells was also required for their efficient clonal expansion by promoting the survival of activated T cells on vaccinia viral infection in vivo. Effector CD8 T cells that lacked direct TLR2-MyD88 signaling did not survive the contraction phase to differentiate into long-lived memory cells. Furthermore, we observed that direct TLR2 ligation on CD8 T cells promoted CD8 T-cell proliferation and survival in vitro in a manner dependent on the phosphatidylinositol 3-kinase (PI3K)-Akt pathway activation and that activation of Akt controlled memory cell formation in vivo. These results identify a critical role for intrinsic TLR2-MyD88 signaling and PI3K-Akt pathway activation in CD8 T-cell clonal expansion and memory formation in vivo and could lead to the development of new vaccine approaches. |
| File Format | PDF HTM / HTML |
| DOI | 10.1182/blood-2008-03-148809 |
| PubMed reference number | 18948575 |
| Journal | Medline |
| Volume Number | 113 |
| Issue Number | 10 |
| Alternate Webpage(s) | http://www.bloodjournal.org/content/bloodjournal/113/10/2256.full.pdf?sso-checked=true |
| Alternate Webpage(s) | https://doi.org/10.1182/blood-2008-03-148809 |
| Journal | Blood |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |