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This study focuses on the development of environmentally friendly Au-Cu 2-x S/CuInS 2 heteronanotrimers. The chosen strategy relies on the laser photodeposition of a single gold nanodot (ND) onto Janus Cu 2- x S/CuInS 2 heteronanocrystals (HNCs). This method offers precise control over the number, location, and size (5 to 8 nm) of the Au NDs by adjusting laser power for the career production, concentration of hole scavenger for charge equilibration in redox reactions, and gold precursor concentration, and exposure time for the final ND size. The photoreduction of gold ions onto HNCs starts systematically at the Cu 2- x S tip. The Au deposition then depends on the CuInS 2 segment length. For short HNCs, stable Au-Cu 2- x S/CuInS 2 heteronanotrimers form, while long HNCs undergo a secondary photo-induced step: the initial Au ND is progressively oxidized, with concomitant deposition of a second gold ND on the CuInS 2 side, to yield Au 2 S-Cu 2- x S/CuInS 2 -Au heteronanotrimers. Results are rationalized by quantitative comparison with a model that describes the growth kinetics of NDs and Au-Cu 2- x S transformation and emphasizes the importance of charge separation in predicting selective deposition in heteronanotrimer production. The key parameter controlling Au-Cu 2‒ x S/CuInS 2 HNCs is the photoinduced electric field gradient generated by charge separation, which is tailored by controlling the CuInS 2 segment size., (© 2024 The Author(s). Small published by Wiley‐VCH GmbH.)

Most of the immunosuppressive effects of interleukin-10 (IL-10) are related to functional inhibition of antigen-presenting cells (APC). Herein, we investigate the influence of recombinant (r)IL-10 on human dendritic cells (DC) purified from peripheral blood of healthy volunteers. First, we found that rIL-10 inhibited in a dose-dependent manner the proliferative responses as well as the production of IL-2 and interferon-gamma (IFN-gamma) in mixed lymphocyte reaction (MLR) between purified T cells and DC. This rIL-10 effect could be attributed to a direct effect on DC, as DC preincubated with rIL-10 were found to be deficient in the induction of alloreactive T cells even when anti-IL-10 neutralizing mAb was added at the time of MLR. Flow cytometric analysis indicated that rIL-10 did not modify the expression of ICAM-1 (CD54) and B7-1 (CD80), but decreased HLA-DR and B7-2 (CD86) expression at the DC surface. We conclude that the inhibitory effect of rIL-10 on primary alloreactive T cell responses involves down-regulation of class II MHC and B7-2 expression at the DC surface.

There is evidence that interleukin -10(IL-10) interferes with the costimulatory properties of antigen-presenting cells and, thereby, inhibits their ability to induce T cell activation. To determine whether this effect might involve modulation of the expression of accessory molecules, we analyzed by flow cytometry the influence of human IL-10 on the basal expression of intercellular adhesion molecule 1 (ICAM-1) as well as on the interferon gamma (IFN-gamma)-induced up-regulation of ICAM-1 and B7 at the surface of human monocytes. IL-10 inhibited both the basal expression and the IFN-gamma-induced ICAM-1 up-regulation. IL-10 also reduced B7 up-regulation on IFN-gamma-stimulated monocytes. The inhibitory effect of IL-10 both on ICAM-1 and B7 expression was shown to be dose dependent. We conclude that the ability of IL-10 to decrease both ICAM-1 and B7 expression on monocytes might contribute to its immunosuppressive properties.

We examined by flow cytometry the expression of lipopolysaccharide (LPS) receptor CD14 molecule on monocytes after addition of LPS to human whole blood. Within 30 min LPS induced an increase in monocyte CD14 expression, peaking between 1 and 3 h and followed by a slow decrease. Maximal increase in anti-CD14 monoclonal antibody binding sites was estimated as twofold the basal value. This effect, already observed with very low concentrations of LPS (10 pg/ml), was dose dependent. Protein synthesis was not involved in the CD14 hyperexpression since it was not influenced by co-incubation with cycloheximide. Finally, LPS-induced up-regulation of monocyte CD14 was associated with an increased binding of fluoresceinated LPS. We conclude that LPS in whole blood up-regulates the expression of its own CD14 receptor on monocytes, a phenomenon that could be relevant to the pathogenesis of gram-negative sepsis.