Beschreibung:
<jats:title>ABSTRACT</jats:title>
<jats:p>
HLA-G is a nonclassical class I human leukocyte antigen (HLA) involved in mechanisms of immune tolerance. The objective of this study was to determine whether
<jats:italic>N</jats:italic>
-(3-oxododecanoyl)-
<jats:sc>l</jats:sc>
-homoserine lactone (3O-C
<jats:sub>12</jats:sub>
-HSL), a quorum sensing molecule produced by
<jats:named-content content-type="genus-species">Pseudomonas aeruginosa</jats:named-content>
, could modify HLA-G expression to control the host immune response. We evaluated the ability of 3O-C
<jats:sub>12</jats:sub>
-HSL to induce HLA-G expression in primary immune cells, monocytes (U937 and THP1), and T-cell lines (Jurkat)
<jats:italic>in vitro</jats:italic>
and analyzed the cellular pathway responsible for HLA-G expression. We studied the HLA-G promoter with a luciferase assay and interleukin-10 (IL-10) and p38/CREB signaling with enzyme-linked immunosorbent assay and immunofluorescence, respectively. We observed that 3O-C
<jats:sub>12</jats:sub>
-HSL is able to induce HLA-G expression in human monocytes and T cells. We showed that the induction of HLA-G by 3O-C
<jats:sub>12</jats:sub>
-HSL is p38/CREB and IL-10 dependent. 3O-C
<jats:sub>12</jats:sub>
-HSL treatment is able to arrest only the U937 cell cycle, possibly due to the peculiar expression of the ILT2 receptor in the U937 cell line. Our observations suggest HLA-G as a mechanism to create a protected niche for the bacterial reservoir, similar to the role of HLA-G molecules during viral infections.
</jats:p>