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EnglishMtb influences DC activity and T cell-mediated immune responses. We show that the treatment of immature monocyte-derived DC with Mtb elicited the formation of mature DC, producing TNF-α, IL-1β, IL-6, and IL-23 and instructing CD4+ cells to secrete IFN-γ and IL-17. Mtb-induced cytokine release by DC depended on dectin-1 receptor engagement, whereas MR or DC-SIGN stimulation inhibited this process. A selective dectin-1 binding by the receptor agonist glucan was sufficient to enable DC to generate Th1/Th17 lymphocytes, showing features comparable with those induced by Mtb-treated DC. Interestingly, DC-SIGN or MR engagement inhibited Th17 and increased Th1 generation by glucan- or Mtb-treated DC. Our results indicate that Mtb modulates the lymphocyte response by affecting DC maturation and cytokine release. Dectin-1 engagement by Mtb enables DC to promote a Th1/Th17 response, whereas DC-SIGN and MR costimulation limits dectin-1-dependent Th17 generation and favors a Th1 response, probably by interfering with release of cytokines.
| Titolo: | Induction of Th1/Th17 immune response by Mycobacterium tuberculosis: role of dectin-1, mannose receptor, and DC-SIGN |
| Autori: | |
| Data di pubblicazione: | 2009 |
| Rivista: | |
| Abstract: | Mtb influences DC activity and T cell-mediated immune responses. We show that the treatment of immature monocyte-derived DC with Mtb elicited the formation of mature DC, producing TNF-α, IL-1β, IL-6, and IL-23 and instructing CD4+ cells to secrete IFN-γ and IL-17. Mtb-induced cytokine release by DC depended on dectin-1 receptor engagement, whereas MR or DC-SIGN stimulation inhibited this process. A selective dectin-1 binding by the receptor agonist glucan was sufficient to enable DC to generate Th1/Th17 lymphocytes, showing features comparable with those induced by Mtb-treated DC. Interestingly, DC-SIGN or MR engagement inhibited Th17 and increased Th1 generation by glucan- or Mtb-treated DC. Our results indicate that Mtb modulates the lymphocyte response by affecting DC maturation and cytokine release. Dectin-1 engagement by Mtb enables DC to promote a Th1/Th17 response, whereas DC-SIGN and MR costimulation limits dectin-1-dependent Th17 generation and favors a Th1 response, probably by interfering with release of cytokines. |
| Handle: | http://hdl.handle.net/11562/338761 |
| Appare nelle tipologie: | 01.01 Articolo in Rivista |
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