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MyD88-dependent TLR1/2 signals educate dendritic cells with gut-specific imprinting properties.

Wang, Sen; Villablanca, Eduardo J; De Calisto, Jaime; Gomes, Daniel C O; Nguyen, Deanna D; Mizoguchi, Emiko; Kagan, Jonathan C; Reinecker, Hans-Christian; Hacohen, Nir; Nagler, Cathryn; Xavier, Ramnik J; Rossi-Bergmann, Bartira; Chen, Yi-Bin; Blomhoff, Rune; Snapper, Scott B; Mora, J Rodrigo.
J Immunol; 187(1): 141-50, 2011 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-21646294
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.
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