Callose is a β-l,3-glucan with diverse roles in the viral pathogenesis of plants. It is widely believed that the deposition of callose and hypersensitive reaction (HR) are critical defence responses of host plants against viral infection. However, the sequence of these two events and their resistance mechanisms are unclear. By exploiting a point inoculation approach combined with aniline blue staining, immuno-electron microscopy and external sphincters staining with tannic acid, we systematically investigated the possible roles of callose deposition during viral infection in soybean. In the incompatible combination, callose deposition at the plasmodesmata (PD) was clearly visible at the sites of inoculation but viral RNA of coat protein (CP-RNA) was not detected by RT-PCR in the leaf above the inoculated one (the upper leaf). In the compatible combination, however, callose deposition at PD was not detected at the site of infection but the viral CP-RNA was detected by RT-PCR in the upper leaf. We also found that in the incompatible combination the fluorescence due to callose formation at the inoculation point disappeared following the injection of 2-deoxy-D-glucose (DDG, an inhibitor of callose synthesis). At same time, in the incompatible combination, necrosis was observed and the viral CP-RNA was detected by RT-PCR in the upper leaf and HR characteristics were evident at the inoculation sites. These results show that, during the defensive response of soybean to viral infection, callose deposition at PD is mainly responsible for restricting the movement of the virus between cells and it occurs prior to the HR response.

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5), and [Pb(NNO) 2 ] (6), have been prepared by the reaction of Pb(NO 3 ) 2 with isonicotinic acid N-oxide (HINO), or nicotinic acid N-oxide (HNNO), and characterized by elemental analysis, IR, and singlecrystal X-ray diffraction. Compound 1, consisting of a one-dimensional (1D) infinite chain, is a three-dimensional (3D) supramolecular framework with a 1D rectanglar channel in which free water molecules locate. The structure of 2 consists of 1D chains built by two parallel INO ligands bridging a pair of rhombic-planar [Pb 2 O 2 ] units, which is further extended into a 2D supramolecular layer via hypervalent interactions and interlayer π-π interactions. Compound 3 consists of a two-dimensional (2D) inorganic layer containing 16-membered rings, which are further linked through µ-INO to generate a unique 3D open framework. In compound 4, the selfassembly based on 2D motifs with side arms leads to the formation of a new type of polythreaded network, which contains 1D channels with guests molecules along the b-axis. In compound 5, NNO ligands in three kinds of coordination modes link to three unique lead centers to generate two kinds of Pb-O chains which are bridged by NNO to give a 2D network. Compound 6 is a 2D layer structure and in the intralayer regions parallel left-and right-handed helical chains exist. In addition, compounds 1, 2, 3, and 6 exhibit strong phosphorescent emissions in the solid state at room temperature. The results of theoretical calculations show that the absorptions of these complexes derive mainly from ligand to ligand charge transfer (LLCT) transitions.

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Summary Follicular T‐helper (TFH) cells play a crucial role in three aspects of the germinal center (GC) response. They promote GC formation, arbitrate competition among GC B cells to determine the outcome of affinity maturation, and regulate GC output of memory and plasma cells to shape the long‐lived humoral immune memory. Of fundamental importance are dynamic physical interactions between TFH and B cells, which are the main platform for TFH cells to deliver “help” factors to B cells and also for reciprocal signaling from B cells to maintain the helper state of TFH cells. Recent work has significantly expanded our understanding of how T‐B interactions are spatiotemporally regulated and molecularly orchestrated to fulfill those TFH functions. In this review, we elaborate two modes of T‐B interactions, the antigen‐specific or cognate mode in which TFH cells engage individual antigen‐presenting B cells and the antigen nonspecific bystander mode in which TFH cells are engaged with the ensemble of follicular B cells. We discuss findings that indicate how short‐lived cognate T‐B contacts coupled with an intercellular positive feedback drive affinity‐based selection and how bystander interactions between T and B cells regulate follicular T‐cell recruitment and maintenance of an appropriate helper state. We argue that this combination of bystander and cognate interactions with B cells constantly shapes the internal state of TFH cells and provides the platform to execute their helper functions.

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