Journal
RETROVIROLOGY
Volume 10, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1742-4690-10-123
Keywords
HIV-1; TLR4; Tat; IL-10; TNF-alpha
Categories
Funding
- ANRS
- SIDACTION
- ministere de la recherche et des technologies
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Background: HIV-1 infection results in hyper-immune activation and immunological disorders as early as the asymptomatic stage. Here, we hypothesized that during early HIV-1 infection, HIV-1 Tat protein acts on monocytes/macrophages to induce anti-inflammatory and proinflammatory cytokines and participates in immune dysregulation. Results: In this work we showed that Tat protein: i) by its N-terminal domain induces production of both IL-10 and TNF-alpha in a TLR4-MD2 dependent manner, ii) interacts specifically with TLR4-MD2 and MD2 with high affinity but not with CD14, iii) induces in vivo TNF-alpha and IL-10 in a TLR4 dependent manner. Conclusions: Collectively, our data showed for the first time that, HIV-1 Tat interacts physically with high affinity with TLR4-MD2 to promote proinflammatory cytokines (TNF-alpha) and the immunosuppressive cytokine IL-10 both involved in immune dysregulation during early HIV-1 infection and AIDS progression.
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