Human Beta Defensin 2 Selectively Inhibits HIV-1 in Highly Permissive CCR6âºCD4⺠T Cells.
Viruses
; 9(5)2017 05 16.
Article
em En
| MEDLINE
| ID: mdl-28509877
ABSTRACT
Chemokine receptor type 6 (CCR6)âºCD4⺠T cells are preferentially infected and depleted during HIV disease progression, but are preserved in non-progressors. CCR6 is expressed on a heterogeneous population of memory CD4⺠T cells that are critical to mucosal immunity. Preferential infection of these cells is associated, in part, with high surface expression of CCR5, CXCR4, and α4ß7. In addition, CCR6âºCD4⺠T cells harbor elevated levels of integrated viral DNA and high levels of proliferation markers. We have previously shown that the CCR6 ligands MIP-3α and human beta defensins inhibit HIV replication. The inhibition required CCR6 and the induction of APOBEC3G. Here, we further characterize the induction of apolipoprotein B mRNA editing enzyme (APOBEC3G) by human beta defensin 2. Human beta defensin 2 rapidly induces transcriptional induction of APOBEC3G that involves extracellular signal-regulated kinases 1/2 (ERK1/2) activation and the transcription factors NFATc2, NFATc1, and IRF4. We demonstrate that human beta defensin 2 selectively protects primary CCR6âºCD4⺠T cells infected with HIV-1. The selective protection of CCR6âºCD4⺠T cell subsets may be critical in maintaining mucosal immune function and preventing disease progression.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Linfócitos T CD4-Positivos
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Infecções por HIV
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HIV-1
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Beta-Defensinas
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Receptores CCR6
Limite:
Humans
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article