Anti-CD4 monoclonal antibody, clone DWT5 [FITC]

A metal-free material was suggested for the photocatalysis of organic dye degradation with a higher catalysis rate based on carbon quantum dots (CQDs) than those for most of previous works. A simple one-pot solvothermal strategy was employed to prepare nitrogen-doped (N-doped) CQDs using different precursors with varying nitrogen contents. As the carbon and nitrogen sources, aniline, 2-aminonaphthalene, 2-anthracylamine, and 1-aminopyrene were used as precursors for the synthesis of four CQDs (abbreviation: CD1, CD2, CD3, CD4), respectively. The fluorescence quantum yield of CQDs all exceeded 0.10, and even arrived at 0.29 for CD3. In addition, the structural, morphological and optical properties of CQDs were characterized by multiple analytical techniques such as X-ray diffraction, transmission electron microscopy, and Fourier transform infrared spectroscopy. CQDs show excellent photocatalytic activity. Four organic dyes including indigo carmine (IC), ethyl violet (EV), congo red (CR), and bordeaux R (Bo-R) were used as models to study the photocatalytic activity of CQDs. Importantly, the degradation efficiency reaches 97% for IC using CD2 under natural light 2 h and the degradation rate constant is 0.0309 min(-1). The results suggest that the present CQDs products have potential applications in the degradation of organic dyes.

Evidence from inflammatory bowel diseases (IBD) patients and animal models has indicated that gut inflammation is driven by effector CD4(+) T-cell, including Th1 and Th17. Conversely, Treg seem to be dysfunctional in IBD. Importantly, dopamine, which is abundant in the gut mucosa under homoeostasis, undergoes a sharp reduction upon intestinal inflammation. Here we analysed the role of the high-affinity dopamine receptor D3 (DRD3) in gut inflammation. Our results show that Drd3 deficiency confers a stronger immunosuppressive potency to Treg, attenuating inflammatory colitis manifestation in mice. Mechanistic analyses indicated that DRD3-signalling attenuates IL-10 production and limits the acquisition of gut-tropism. Accordingly, the ex vivo transduction of wild-type Treg with a siRNA for Drd3 induced a potent therapeutic effect abolishing gut inflammation. Thus, our findings show DRD3-signalling as a major regulator of Treg upon gut inflammation.