A new facile method for preparing water-soluble near-infrared （NIR）-emitting PbS quantum dots （QDs） is proposed by using N-acetyl-L-cysteine （NAC, a derivate of L-cysteine） as its stabilizer. The influence of the precursor Pb/S molar ratio, the Pb/NAC molar ratio, and the pH of original solution on optical properties is explored. Results show that aqueous PbS QDs with strong NIR fluorescence can be prepared and their photoluminescence emission peaks can be tuned from 895 nm to 970 nm. Studies indicate that such aqueous QDs have a potential application in biomedical imaging, especially in noninvasive in vivo fluorescence imaging. In addition, the resulting PbS QDs are further characterized by a transmission electron microscopy and X-ray diffraction analysis.
T cell immunoglobulin and mucin domain 3 （Tim-3） is well known to negatively regulate T cells responses, but its role in burn-induced T cells immune suppression remains unclear. In the present study, in order to identify the relationship between Tim-3 expression and post-burn T cells immune suppression, C57BL/6 mice were subjected to burn injury or sham injury, and the liver and spleen were harvested at the day 1 after operation. The expression level of Tim-3 on hepatic or splenic T cells and the functional properties of Tim-3＋ T cells were evaluated. It was found burn injury induced dramatically elevated Tim-3 expression on both hepatic and splenic CD4＋ and CD8＋ T cells in contrast with the post-burn depletion of T cells. Furthermore, Tim-3 expression was correlated with the suppressive phenotype of T cells following burn injury, including increased expression of anti-inflammatory cytokine IL-10, decreased expression of pro-inflammatory cytokines IFN-γ and TNF-α, reduced T cell proliferation and elevated co-expression of Tim-3 and PD-1. Moreover, Tim-3＋ T cells subsets were more prone to spontaneous apoptosis than Tim-3- T cells subsets. Our findings reinforce the idea that the up-regulated expression of Tim-3 on T cells after burn injury plays an important role in the development and maintenance of burn-induced T cell immune suppression.
