Journal
VIRUSES-BASEL
Volume 9, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/v9050111
Keywords
defensins; viruses; immune response; HIV; CCR6; pathogenesis; human beta defensin 2; Th17
Categories
Funding
- National Institute of Neurological Disorders And Stroke [R01NS066842]
- National Institute of Allergy and Infectious Diseases [1T32AI095190-01A1, T32AI007540]
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Chemokine receptor type 6 (CCR6)(+)CD4(+) 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(+) 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 alpha 4 beta 7. In addition, CCR6(+)CD4(+) T cells harbor elevated levels of integrated viral DNA and high levels of proliferation markers. We have previously shown that the CCR6 ligands MIP-3 alpha 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 CCR6(+)CD4(+) T cells infected with HIV-1. The selective protection of CCR6(+)CD4(+) T cell subsets may be critical in maintaining mucosal immune function and preventing disease progression.
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