| pubmed-article:19252500 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C0014442 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C0042890 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C0670896 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C0004368 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C0220905 | lld:lifeskim |
| pubmed-article:19252500 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:19252500 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19252500 | pubmed:dateCreated | 2009-4-7 | lld:pubmed |
| pubmed-article:19252500 | pubmed:abstractText | Immune sensing of a microbe occurs via multiple receptors. How signals from different receptors are coordinated to yield a specific immune response is poorly understood. We show that two pathogen recognition receptors, Toll-like receptor 2 (TLR2) and dectin-1, recognizing the same microbial stimulus, stimulate distinct innate and adaptive responses. TLR2 signaling induced splenic dendritic cells (DCs) to express the retinoic acid metabolizing enzyme retinaldehyde dehydrogenase type 2 and interleukin-10 (IL-10) and to metabolize vitamin A and stimulate Foxp3(+) T regulatory cells (T(reg) cells). Retinoic acid acted on DCs to induce suppressor of cytokine signaling-3 expression, which suppressed activation of p38 mitogen-activated protein kinase and proinflammatory cytokines. Consistent with this finding, TLR2 signaling induced T(reg) cells and suppressed IL-23 and T helper type 17 (T(H)17) and T(H)1-mediated autoimmune responses in vivo. In contrast, dectin-1 signaling mostly induced IL-23 and proinflammatory cytokines and augmented T(H)17 and T(H)1-mediated autoimmune responses in vivo. These data define a new mechanism for the systemic induction of retinoic acid and immune suppression against autoimmunity. | lld:pubmed |
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