Abstract
Monocytes play critical roles in human immunodeficiency virus type-1 (HIV-1) pathogenesis. During HIV-1 infection, proinflammatory molecules such as prostaglandin E2 (PGE2) are observed at elevated levels in infected individuals.
Highlights
Transmission and pathogenesis of the Human Immunodeficiency Virus type-1 (HIV-1) are interconnected during all stages of the disease with cells of the monocyte/macrophage lineage [1,2,3]
Surface expression of CCR7 on HIV-1 exposed human monocytes is modulated by prostaglandin E2 (PGE2)
The addition of PGE2 to HIV-1-exposed Mono-Mac-1 was associated with an increase of CCR7 expression compared to PGE2-treated uninfected cells
Summary
Transmission and pathogenesis of the Human Immunodeficiency Virus type-1 (HIV-1) are interconnected during all stages of the disease with cells of the monocyte/macrophage lineage [1,2,3]. Monocytes arising from quiescent and infected cells of the myeloid precursor lineage in bone marrow have been demonstrated as a source of residual HIV DNA [1,7,9,10,11,12]. CCL19 and CCL21 are the natural ligands of CCR7, which is expressed on DCs [19] and on T and B cells [20,21,22] as well as on monocytes [23]. In human monocytes and DCs, prostaglandin E2 (PGE2), a pleiotropic immunomodulatory molecule, exerts multiple effects on both CCR7 expression level and functionality [23,26,27]
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