Activation of Toll-like receptor 2 increases macrophage resistance to HIV-1 infection.
Immunobiology
; 218(12): 1529-36, 2013 Dec.
Article
em En
| MEDLINE
| ID: mdl-23891328
Patients infected with HIV-1, the etiological agent of AIDS, have increased intestinal permeability, which allows for the passage of microbial products, including Toll-like receptor (TLR) ligands, into circulation. The exposure of HIV-1-infected cells to certain TLR agonists affects viral replication, but studies associating viral production with the activation of TLR2 in HIV-1-infected cells are rare and controversial. Here, we report that the TLR2 ligands Zymosan and Pam3CSK4 potently inhibit HIV-1 replication in acutely infected monocyte-derived macrophages and the exposure to TLR2 ligands prior to infection renders macrophages refractory to HIV-1 production. Macrophage treatment with Pam3CSK4 did not change the cellular expression of the HIV-1 entry receptors CD4 and CCR5. Both TLR2 ligands increased the macrophage production of ß-chemokines and IL-10, and the blockage of these soluble factors prevented the inhibitory effect of TLR2 activation on HIV-1 replication. Our findings show that the direct engagement of TLR2 in HIV-1-infected macrophages increase cellular resistance to HIV-1 infection, and that controlling HIV-1 replication with agonists for TLR2 might have implications for the development of antiretroviral therapies.
Palavras-chave
AIDS; HIV; HIV-1; IL; IL-10; LPS; Macrophages; PAMP; PBMCs; PHA; TLR; Toll-like receptor; Toll-like receptors.; acquired immunodeficiency syndrome; human immunodeficiency virus type-1; interleukin; lipopolysaccharide; pathogen-associated molecular patterns; peripheral blood mononuclear cells; phytohemagglutinin; ß-Chemokines
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Antivirais
/
Zimosan
/
Infecções por HIV
/
HIV-1
/
Receptor 2 Toll-Like
/
Lipopeptídeos
/
Macrófagos
Limite:
Humans
Idioma:
En
Revista:
Immunobiology
Ano de publicação:
2013
Tipo de documento:
Article
País de afiliação:
Brasil
País de publicação:
Holanda