This tutorial review focuses on the modification and assembly of atomically-precise silver clusters by changing shell layers for more stability and functionalities, especially for brighter luminescence.

Chiral assembly and asymmetric synthesis are critically important for the generation of chiral metal clusters with chiroptical activities. Here, a racemic mixture of [K(CH3OH)2(18‐crown‐6)]+[Cu5(StBu)6]− (1⋅CH3OH) in the chiral space group was prepared, in which the chiral red‐emissive anionic [Cu5(StBu)6]− cluster was arranged along a twofold screw axis. Interestingly, the release of the coordinated CH3OH of the cationic units turned the chiral 1⋅CH3OH crystal into a mesomeric crystal [K(18‐crown‐6)]+[Cu5(StBu)6]− (1), which has a centrosymmetric space group, by adding symmetry elements of glide and mirror planes through both disordered [Cu5(StBu)6]− units. The switchable chiral/achiral rearrangement of [Cu5(StBu)6]− clusters along with the capture/release of CH3OH were concomitant with an intense increase/decrease in luminescence. We also used cationic chiral amino alcohols to induce the chiral assembly of a pair of enantiomers, [d/l‐valinol(18‐crown‐6)]+[Cu5(StBu)6]− (d/l‐Cu5V), which display impressive circularly polarized luminescence (CPL) in contrast to the CPL‐silent racemic mixture of 1⋅CH3OH and mesomeric 1.

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During 1 year, we used immunocytochemical staining of human cerebellum to screen 1,488 serums for IgG autoantibodies to Hu and Yo antigens. Three serums had none of the classically described patterns of IgG binding but instead, selectively stained the cerebellar molecular layer. Evaluation of clinical data showed that the patients had either typical Miller Fisher syndrome (MFS) or Guillain-Barré syndrome with ophthalmoplegia. Further analysis by ELISA, assay showed that all three serums had high titers of IgG anti-GQ1b autoantibodies. IgG autoantibody staining of human cerebellum, which is used for the diagnosis of paraneoplastic disorders, may have additional specificity for other, presumably autoimmune, syndromes such as MFS. The specificity of the serum IgG autoantibody binding to the cerebella molecular layer may be related to the ataxia that often occurs in these patients.

Tumor heterogeneity has been associated with immunotherapy and targeted drug resistance in hepatocellular carcinoma (HCC). However, communications between tumor and cytotoxic cells are poorly understood to date. In the present study, thirty-one clusters of cells were discovered in the tumor tissues and adjacent tissues through single-cell sequencing. Moreover, the quantity and function exhaustion of cytotoxic cells was observed to be induced in tumors by the TCR and apoptosis signal pathways. Furthermore, granzyme failure of cytotoxic cells was observed in HCC patients. Importantly, the GZMA secreted by cytotoxic cells was demonstrated to interact with the F2R expressed by the tumor cells both in vivo and in vitro. This interaction induced tumor suppression and T cell-mediated killing of tumor cells via the activation of the JAK2/STAT1 signaling pathway. Mechanistically, the activation of JAK2/STAT1 signaling promoted apoptosis under the mediating effect of the LDPRSFLL motif at the N-terminus of F2R, which interacted with GZMA. In addition, GZMA and F2R were positively correlated with PD-1 and PD-L1 in tumor tissues, while the expressions of F2R and GZMA promoted PD-1 mAb-induced tumor suppression in both mouse model and HCC patients. Finally, in HCC patients, a low expression of GZMA and F2R in the tumor tissues was correlated with aggressive clinicopathological characteristics and poor prognosis. Collectively, GZMA-F2R communication inefficient induces deficient PD-1 mAb therapy and provide a completely novel immunotherapy strategy for tumor suppression in HCC patients.