The Spiro-OMeTAD is one of the most widely used hole transport materials in highly efficient perovskite solar cells (PSCs), whose performance typically relies on dopants such as lithium bis(trifluoromethanesulfonyl)imide (LiTFSI) and 4-tert-butylpyridine (TBP) to enhance conductivity and hole transport efficiency. However, these conventional dopants suffer from high volatility and hygroscopicity, severely limiting the long-term stability and commercialization potential of PSCs. To solve this problem, this work developed a novel dopant 4-isopropyl-4′-methyldiphenyl iodide tetrakis(pentafluorophenyl)borate (IMT) as a substitute for LiTFSI and TBP for synergistic doping regulation of Spiro-OMeTAD. It was revealed that IMT possessed a well-delocalized electronic structure and appropriately aligned energy levels, which effectively promoted the oxidation of Spiro-OMeTAD, thereby enhancing its electrical conductivity and hole mobility. Additionally, the incorporation of IMT improved the hydrophobicity and compactness of the Spiro-OMeTAD film, effectively mitigating moisture penetration and suppressing interfacial ion migration. The rigid and flexible PSCs based on IMT doping exhibited excellent optoelectronic performance, with the champion power conversion efficiencies reaching 24.97 % and 23.15 %, respectively, which were significantly higher than those of conventional devices using LiTFSI and TBP as dopants. More importantly, the introduction of IMT effectively improved the environmental stability of perovskite devices, enabling them to maintain high-efficiency output under high humidity, high temperature and long-term illumination conditions. This work proposes a new doping strategy for efficient, stable and LiTFSI/TBP-independent PSCs, and provides a theoretical and practical basis for the molecular design of hole transport materials.
Tumor immunotherapy has shown great progress for the treatment of cancer; however, both endogenous and exogenous T cells are inhibited by the immunosuppressive tumor microenvironment. Tumor-associated macrophages (TAMs) in the microenvironment play pivotal and complex roles in tumor development and progression. Macrophages are categorized as M1 and M2 types. Relevant studies suggest that M2 TAMs correlate with poor prognosis. Colony-stimulating factor 1 receptor (CSF1R) controls the formation, differentiation and function of M2 macrophages, which helps tumors grow, metastasize and secrete immunosuppressive cytokines. The objectives of this study were to establish two types of third-generation chimeric antigen receptors (CARs) that could specifically target human CSF1R, and to introduce the CARs into NK92MI cells and normal human peripheral blood T cells through lentiviral transduction to produce CAR-natural killer (NK) and -T cells. We then tested their cytotoxicity against cell lines and peripheral blood monocytes expressing CSF1R. In vitro experiments confirmed that third-generation CARs had good target specificity and cytotoxicity. It was expected that CAR-NK and -T cells could specifically kill M2 TAMs in the tumor microenvironment and remove their inhibitory effect. Therefore, CSF1R-targeting CAR-NK and -T cells could represent a novel cellular immunotherapy strategy in conjunction with other antibody-based drugs and targeted therapeutics.
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