| First Author | Wang S | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 1 | Pages | 141-50 |
| PubMed ID | 21646294 | Mgi Jnum | J:176180 |
| Mgi Id | MGI:5288582 | Doi | 10.4049/jimmunol.1003740 |
| Citation | Wang S, et al. (2011) MyD88-dependent TLR1/2 signals educate dendritic cells with gut-specific imprinting properties. J Immunol 187(1):141-50 |
| abstractText | Gut-associated dendritic cells (DC) synthesize all-trans retinoic acid, which is required for inducing gut-tropic lymphocytes. Gut-associated DC from MyD88(-/-) mice, which lack most TLR signals, expressed low levels of retinal dehydrogenases (critical enzymes for all-trans retinoic acid biosynthesis) and were significantly impaired in their ability to induce gut-homing T cells. Pretreatment of extraintestinal DC with a TLR1/2 agonist was sufficient to induce retinal dehydrogenases and to confer these DC with the capacity to induce gut-homing lymphocytes via a mechanism dependent on MyD88 and JNK/MAPK. Moreover, gut-associated DC from TLR2(-/-) mice, or from mice in which JNK was pharmacologically blocked, were impaired in their education to imprint gut-homing T cells, which correlated with a decreased induction of gut-tropic T cells in TLR2(-/-) mice upon immunization. Thus, MyD88-dependent TLR2 signals are necessary and sufficient to educate DC with gut-specific imprinting properties and contribute in vivo to the generation of gut-tropic T cells. |
