Fluorescence imaging sheds light on the immune evasion mechanisms of hepatic stellate cells mediated by superoxide anion.

Whether and how the reactive oxygen species generated by hepatic stellate cells (HSCs) promote immune evasion of hepatocellular carcinoma (HCC) remains mysterious. Therefore, investigating the function of superoxide anion (O2•-), the firstly generated reactive oxygen species, during the immune evasion become necessary. In this work, we establish a novel in situ imaging method for visualization of O2•- changes in HSCs based on a new two-photon fluorescence probe TPH. TPH comprises recognition group for O2•- and HSCs targeting peptides. We observe that O2•- in HSCs gradually rose, impairing the infiltration of CD8+ T cells in HCC mice. Further studies reveal that the cyclin-dependent kinase 4 is deactivated by O2•-, and then cause the up-regulation of PD-L1. Our work provides molecular insights into HSC-mediated immune evasion of HCC, which may represent potential targets for HCC immunotherapy.

Remarkable emission enhancement of CsPbBr3 quantum dots based on an Ag nanoparticle-Ag film plasmonic coupling structure.

All-inorganic halide perovskite quantum dots (QDs) have recently received much attention due to their excellent optoelectronic properties. And their emission properties still need to be improved for further applications. Here, we demonstrated a remarkable emission enhancement of the CsPbBr3 QDs based on an Ag nanoparticle-Ag film plasmonic coupling structure. Through precise control of the gap distance between Ag nanoparticle and Ag film, the localized surface plasmon resonance (LSPR) peak was tuned to match the emission wavelength of the CsPbBr3 QDs. We achieved a 30-fold fluorescence intensity enhancement and a lower lasing threshold, which is 25% of that of the CsPbBr3 QDs without plasmonic coupling structure. It is attributed to that the plasmonic coupling structure exhibits an extremely strong local electric field owing to the coupling between LSPR of Ag nanoparticle and surface plasmon polariton of Ag film. This work provides an effective way to enhance the optical emission of perovskite QDs and promotes the further exploration of on-chip light source.

Study on Magnetic and Plasmonic Properties of Fe3O4-PEI-Au and Fe3O4-PEI-Ag Nanoparticles.

Magnetic-plasmonic nanoparticles (NPs) have attracted great interest in many fields because they can exhibit more physical and chemical properties than individual magnetic or plasmonic NPs. In this work, we synthesized Au- or Ag-decorated Fe3O4 nanoparticles coated with PEI (Fe3O4-PEI-M (M = Au or Ag) NPs) using a simple method. The influences of the plasmonic metal NPs' (Au or Ag) coating density on the magnetic and plasmonic properties of the Fe3O4-PEI-M (M = Au or Ag) NPs were investigated, and the density of the plasmonic metal NPs coated on the Fe3O4 NPs surfaces could be adjusted by controlling the polyethyleneimine (PEI) concentration. It showed that the Fe3O4-PEI-M (M = Au or Ag) NPs exhibited both magnetic and plasmonic properties. When the PEI concentration increased from 5 to 35 mg/mL, the coating density of the Au or Ag NPs on the Fe3O4 NPs surfaces increased, the corresponding magnetic intensity became weaker, and the plasmonic intensity was stronger. At the same time, the plasmonic resonance peak of the Fe3O4-PEI-M (M = Au or Ag) NPs was red shifted. Therefore, there was an optimal coverage of the plasmonic metal NPs on the Fe3O4 NPs surfaces to balance the magnetic and plasmonic properties when the PEI concentration was between 15 and 25 mg/mL. This result can guide the application of the Fe3O4-M (M = Au or Ag) NPs in the biomedical field.

Preparation of TiO2/SnO2 Electron Transport Layer for Performance Enhancement of All-Inorganic Perovskite Solar Cells Using Electron Beam Evaporation at Low Temperature.

SnO2 has attracted much attention due to its low-temperature synthesis (ca. 140 °C), high electron mobility, and low-cost manufacturing. However, lattice mismatch and oxygen vacancies at the SnO2/CsPbI3-xBrx interface generally lead to undesirable nonradiative recombination in optoelectronic devices. The traditional TiO2 used as the electron transport layer (ETL) for all-inorganic perovskite solar cells (PSCs) requires high-temperature sintering and crystallization, which are not suitable for the promising flexible PSCs and tandem solar cells, raising concerns about surface defects and device uniformity. To address these challenges, we present a bilayer ETL consisting of a SnO2 layer using electron beam evaporation and a TiO2 layer through the hydrothermal method, resulting in an enhanced performance of the perovskite solar cell. The bilayer device exhibits an improved power conversion efficiency of 11.48% compared to the single-layer device (8.09%). The average fill factor of the bilayer electron transport layer is approximately 15% higher compared to the single-layer electron transport layer. Through a systematic investigation of the use of ETL for CsPb3-xBrx PSCs on optical and electronic properties, we demonstrate that the SnO2/TiO2 is an efficient bilayer ETL for PSCs as it significantly enhances the charge extraction capability, suppresses carrier recombination at the ETL/perovskite interface, facilitates efficient photogenerated carrier separation and transport, and provides high current density and reduced hysteresis.

Defective LAT signalosome pathology in mice mimics human IgG4-related disease at single-cell level.

Mice with a loss-of-function mutation in the LAT adaptor (LatY136F) develop an autoimmune and type 2 inflammatory disorder called defective LAT signalosome pathology (DLSP). We analyzed via single-cell omics the trajectory leading to LatY136F DLSP and the underlying CD4+ T cell diversification. T follicular helper cells, CD4+ cytotoxic T cells, activated B cells, and plasma cells were found in LatY136F spleen and lung. Such cell constellation entailed all the cell types causative of human IgG4-related disease (IgG4-RD), an autoimmune and inflammatory condition with LatY136F DLSP-like histopathological manifestations. Most previously described T cell-mediated autoimmune manifestations require persistent TCR input. In contrast, following their first engagement by self-antigens, the autoreactive TCR expressed by LatY136F CD4+ T cells hand over their central role in T cell activation to CD28 costimulatory molecules. As a result, all subsequent LatY136F DLSP manifestations, including the production of autoantibodies, solely rely on CD28 engagement. Our findings elucidate the etiology of the LatY136F DLSP and qualify it as a model of IgG4-RD.

Boosting the Performance of Perovskite Solar Cells through Systematic Investigation of the Annealing Effect of E-Beam Evaporated TiO2.

Electron transport layer (ETL) plays an undeniable role in improving the performance of n-i-p planar perovskite solar cells (PSCs). Titanium dioxide (TiO2) is known as a promising ETL material for perovskite solar cell. In this work, the effect of annealing temperature on optical, electrical, and surface morphology of the electron-beam (EB)-evaporated TiO2 ETL, and consequently on the performance of perovskite solar cell, was investigated. It was found that annealing treatment at an optimized temperature of 480 °C considerably improved the surface smoothness, density of grain boundaries, and carrier mobility of TiO2 film, which resulted in nearly 10-fold improvement in power conversion efficiency (11.16%) in comparison with the unannealed device (1.08%). The improvement in performance of the optimized PSC is attributed to the acceleration of charge carrier extraction, as well as suppression of the recombination at the ETL/Perovskite interface.

High-performance all-inorganic CsPbBr3 quantum dots with a low-threshold amplified spontaneous emission.

All-inorganic halide perovskite CsPbX3(X = Br/Cl/I)quantum dots have gained a considerable attention in the optoelectronic fields. However, the high cost and poor stability of the prepared CsPbX3 quantum dots (QDs) are inevitable challenges for their future practical applications. And the high-performance CsPbX3 QDs are always needed. Herein, a facile and low-cost synthesis scheme was adopted to prepare the CsPbBr3 QDs modified by lead bromide (PbBr2) and tetraoctylammonium bromide (TOAB) ligands at room temperature in open air. The prepared CsPbBr3 QDs exhibited a high photoluminescence quantum yield (PLQY) of 96.6% and a low amplified spontaneous emission (ASE) threshold of 12.6 µJ/cm2. Stable ASE intensity with little degradation was also realized from the CsPbBr3 QDs doped with PMMA. Furthermore, the enhanced ASE properties of the CsPbBr3 QDs-doped PMMA based on distributed feedback (DFB) substrate was achieved with a lower threshold of 3.6 µJ/cm2, which is 28.6% of that of the (PbBr2 + TOAB)-treated CsPbBr3 QDs without PMMA. This work exhibits a promising potential in the on-chip light source.

Mutation of the glycine residue preceding the sixth tyrosine of the LAT adaptor severely alters T cell development and activation.

The LAT transmembrane adaptor is essential to transduce intracellular signals triggered by the TCR. Phosphorylation of its four C-terminal tyrosine residues (136, 175, 195, and 235 in mouse LAT) recruits several proteins resulting in the assembly of the LAT signalosome. Among those tyrosine residues, the one found at position 136 of mouse LAT plays a critical role for T cell development and activation. The kinetics of phosphorylation of this residue is delayed as compared to the three other C-terminal tyrosines due to a conserved glycine residue found at position 135. Mutation of this glycine into an aspartate residue (denoted LATG135D) increased TCR signaling and altered antigen recognition in human Jurkat T cells and ex vivo mouse T cells. Here, using a strain of LATG135D knockin mice, we showed that the LATG135D mutation modifies thymic development, causing an increase in the percentage of CD4+CD8+ double-positive cells, and a reduction in the percentage of CD4+ and CD8+ single-positive cells. Interestingly, the LATG135D mutation alters thymic development even in a heterozygous state. In the periphery, the LATG135D mutation reduces the percentage of CD8+ T cells and results in a small increment of γδ T cells. Remarkably, the LATG135D mutation dramatically increases the percentage of central memory CD8+ T cells. Finally, analysis of the proliferation and activation of T lymphocytes shows increased responses of T cells from mutant mice. Altogether, our results reinforce the view that the residue preceding Tyr136 of LAT constitutes a crucial checkpoint in T cell development and activation.

Excessive immunosuppression by regulatory T cells antagonizes T cell response to schistosome infection in PD-1-deficient mice.

Schistosomiasis is caused by parasitic flatworms known as schistosomes and affects over 200 million people worldwide. Prevention of T cell exhaustion by blockade of PD-1 results in clinical benefits to cancer patients and clearance of viral infections, however it remains largely unknown whether loss of PD-1 could prevent or cure schistosomiasis in susceptible mice. In this study, we found that S. japonicum infection dramatically induced PD-1 expression in T cells of the liver where the parasites chronically inhabit and elicit deadly inflammation. Even in mice infected by non-egg-producing unisex parasites, we still observed potent induction of PD-1 in liver T cells of C57BL/6 mice following S. japonicum infection. To determine the function of PD-1 in schistosomiasis, we generated PD-1-deficient mice by CRISPR/Cas9 and found that loss of PD-1 markedly increased T cell count in the liver and spleen of infected mice. IL-4 secreting Th2 cells were significantly decreased in the infected PD-1-deficient mice whereas IFN-γ secreting CD4+ and CD8+ T cells were markedly increased. Surprisingly, such beneficial changes of T cell response did not result in eradication of parasites or in lowering the pathogen burden. In further experiments, we found that loss of PD-1 resulted in both beneficial T cell responses and amplification of regulatory T cells that prevented PD-1-deficient T cells from unleashing anti-parasite activity. Moreover, such PD-1-deficient Tregs exert excessive immunosuppression and express larger amounts of adenosine receptors CD39 and CD73 that are crucial for Treg-mediated immunosuppression. Our experimental results have elucidated the function of PD-1 in schistosomiasis and provide novel insights into prevention and treatment of schistosomiasis on the basis of modulating host adaptive immunity.

A Murine Point Mutation of Sgpl1 Skin Is Enriched With Vγ6 IL17-Producing Cell and Revealed With Hyperpigmentation After Imiquimod Treatment.

Sphingosine-1-phosphate lyase is encoded by the Sgpl1 gene, degrades S1P, and is crucial for S1P homeostasis in animal models and humans. S1P lyase deficient patients suffer from adrenal insufficiency, severe lymphopenia, and skin disorders. In this study, we used random mutagenesis screening to identify a mouse line carrying a missense mutation of Sgpl1 (M467K). This mutation caused similar pathologies as Sgpl1 knock-out mice in multiple organs, but greatly preserved its lifespan, which M467K mutation mice look normal under SPF conditions for over 40 weeks, in contrast, the knock-out mice live no more than 6 weeks. When treated with Imiquimod, Sgpl1M467K mice experienced exacerbated skin inflammation, as revealed by aggravated acanthosis and orthokeratotic hyperkeratosis. We also demonstrated that the IL17a producing Vγ6+ cell was enriched in Sgpl1M467K skin and caused severe pathology after imiquimod treatment. Interestingly, hyperchromic plaque occurred in the mutant mice one month after Imiquimod treatment but not in the controls, which resembled the skin disorder found in Sgpl1 deficient patients. Therefore, our results demonstrate that Sgpl1M467K point mutation mice successfully modeled a human disease after being treated with Imiquimod. We also revealed a major subset of γδT cells in the skin, IL17 secreting Vγ6 T cells were augmented by Sgpl1 deficiency and led to skin pathology. Therefore, we have, for the first time, linked the IL17a and γδT cells to SPL insufficiency.

ARHGAP45 controls naïve T- and B-cell entry into lymph nodes and T-cell progenitor thymus seeding.

T and B cells continually recirculate between blood and secondary lymphoid organs. To promote their trans-endothelial migration (TEM), chemokine receptors control the activity of RHO family small GTPases in part via GTPase-activating proteins (GAPs). T and B cells express several RHO-GAPs, the function of most of which remains unknown. The ARHGAP45 GAP is predominantly expressed in hematopoietic cells. To define its in vivo function, we describe two mouse models where ARHGAP45 is ablated systemically or selectively in T cells. We combine their analysis with affinity purification coupled to mass spectrometry to determine the ARHGAP45 interactome in T cells and with time-lapse and reflection interference contrast microscopy to assess the role of ARGHAP45 in T-cell polarization and motility. We demonstrate that ARHGAP45 regulates naïve T-cell deformability and motility. Under physiological conditions, ARHGAP45 controls the entry of naïve T and B cells into lymph nodes whereas under competitive repopulation it further regulates hematopoietic progenitor cell engraftment in the bone marrow, and T-cell progenitor thymus seeding. Therefore, the ARGHAP45 GAP controls multiple key steps in the life of T and B cells.

Characteristics of planktonic and sediment bacterial communities in a heavily polluted urban river.

Urban rivers represent a unique ecosystem in which pollution occurs regularly, altering the biogeochemical characteristics of waterbodies and sediments. However, little is presently known about the spatiotemporal patterns of planktonic and sediment bacterial community diversities and compositions in urban rivers. Herein, Illumina MiSeq high-throughput sequencing was performed to reveal the spatiotemporal dynamics of bacterial populations in Liangtan River, a heavily polluted urban river in Chongqing City (China). The results showed the richness and diversity of sediment bacteria were significantly higher than those of planktonic bacteria, whereas a strong overlap (46.7%) in OTUs was identified between water and sediment samples. Bacterial community composition remarkably differed in waters and sediments. Planktonic bacterial communities were dominated by Proteobacteria, Bacteroidetes, Cyanobacteria and Actinobacteria, while sediment bacterial communities mainly included Proteobacteria, Actinobacteria, Chloroflexi and Bacteroidetes. Additionally, several taxonomic groups of potential bacterial pathogens showed an increasing trend in water and sediment samples from residential and industrial areas (RI). Variation partition analysis (VPA) indicated that temperature and nutrient were identified as the main drivers determining the planktonic and sediment bacterial assemblages. These results highlight that bacterial communities in the polluted urban river exhibit spatiotemporal variation due to the combined influence of environmental factors associated with sewage discharge and hydropower dams.

Structures, Mobilities, and Electronic Properties of Functionalized Silicene: Superhalogen BO2 Adsorption.

The narrow band gap of silicene severely hinders its application in nanoelectronic devices. Therefore, it is significant to open the band gap of silicene and maintain its high carrier mobility. And for that, the adsorption of different coverage superhalogens BO2 on the silicene surface have been investigated based on density functional theory and the CALYPSO method. The results show that BO2 unit prefers to adsorb on silicene with adjacent mode irrespective of the size of substrate. The electronic structure analysis indicates that the density of states near the Fermi level are mainly contributed by Si-p and BO2-p orbitals. (BO2)n-silicene exhibits metallic character with the exception of (BO2)2 adsorbed on 4 × 4 supercell. As for (BO2)2-silicene, silicene transforms from a gapless direct semiconductor to an indirect semiconductor. Furthermore, the effective electron mass of two BO2 superhalogens on 4 × 4 silicene is estimated and found to be smaller than that of graphene. It is expected to result in higher electron mobility.

Tetraethylenepent-MAPbI3-xClx Unsymmetrical Structure-Enhanced Stability and Power Conversion Efficiency in Perovskite Solar Cells.

Two-dimensional (2D) perovskite solar cell (PSC) can achieve high stability by alternating interface cations. However, its main transmissive charge is limited owing to the 2D structure. Therefore, compared with a 3D device, the 2D PSC has poor power conversion efficiency (PCE). Further enhanced performance will require an increase in the transmission dimension of 2D PSC. Here, a novel tetraethylenepent (TEPA)-MAPbI3-xClx analogous 2D unsymmetrical perovskite film was developed to improve the stability and PCE of the corresponding device. Based on the interaction of the active amino linear short chain of TEPA and the halogen ion, the symmetry of the mechanical structure of ions is disrupted, and the TEPA ion is embedded in the perovskite structure to form a perovskite structure with a dimension between 3D and 2D. Noticeably, the TEPA-MAPbI3-xClx devices deliver high PCEs up to 19.73% which stands as the highest for MAPbI3-xClx-based PSC. The environmental, thermal, and illumination stability also showed improvements ranging between 10%-30%. The enhanced PSCs are due to the higher quality of perovskite films, stronger charge transmission, and less trap density. This approach provides a new method to improve and modify 2D PSCs.

Specific Decrease in B-Cell-Derived Extracellular Vesicles Enhances Post-Chemotherapeutic CD8+ T Cell Responses.

Systemic immunosuppression greatly affects the chemotherapeutic antitumor effect. Here, we showed that CD19+ extracellular vesicles (EVs) from B cells through CD39 and CD73 vesicle-incorporated proteins hydrolyzed ATP from chemotherapy-treated tumor cells into adenosine, thus impairing CD8+ T cell responses. Serum CD19+ EVs were increased in tumor-bearing mice and patients. Patients with fewer serum CD19+ EVs had a better prognosis after chemotherapy. Upregulated hypoxia-inducible factor-1α (HIF-1α) promoted B cells to release CD19+ EVs by inducing Rab27a mRNA transcription. Rab27a or HIF-1α deficiency in B cells inhibited CD19+ EV production and improved the chemotherapeutic antitumor effect. Silencing of Rab27a in B cells by inactivated Epstein-Barr viruses carrying Rab27a siRNA greatly improved chemotherapeutic efficacy in humanized immunocompromised NOD PrkdcscidIl2rg-/- mice. Thus, decreasing CD19+ EVs holds high potential to improve the chemotherapeutic antitumor effect.

Post-transcriptional regulator Rbm47 elevates IL-10 production and promotes the immunosuppression of B cells.

Regulatory B cells (Bregs) are a functionally defined B cell subset, and IL-10 is crucial for the suppressive functions of Bregs. However, little is known regarding how IL-10 production is regulated in B cells. To explore the mechanisms by which IL-10 is regulated in B cells, we used mRNA microarrays to screen for molecules that are upregulated in IL-10-producing B cells and identified RNA-binding motif protein 47 (Rbm47) as a post-transcriptional regulator. Rbm47 was found to promote IL-10 production in B cells. We found that Rbm47 promotes the stability of IL-10 mRNA by binding to AU-rich elements in the 3' untranslated region of Il10 mRNA. In addition, we demonstrated that the overexpression of Rbm47 enabled B cells to facilitate Foxp3+ regulator T-cell induction and reduce the severity of DSS-induced ulcerative colitis. Taken together, these results suggest that Rbm47 plays an important role in regulating IL-10 at the post-transcriptional level, thus promoting the regulatory functions of B cells. The findings presented in this study not only increase our understanding of the post-translational regulation of IL-10 in B cells but also identify a novel strategy for the potential application of Bregs.

CD69 enhances immunosuppressive function of regulatory T-cells and attenuates colitis by prompting IL-10 production.

Foxp3+ regulatory T cells (Tregs) can inhibit immune responses and maintain immune tolerance by secreting immunosuppressive TGF-ß1 and IL-10. However, the efficiency of Tregs become the major obstacle to their use for immunotherapy. In this study, we investigated the relevance of the C-type lectin receptor CD69 to the suppressive function. Compared to CD4+Foxp3+CD69- Tregs (CD69- Tregs), CD4+Foxp3+CD69+ Tregs (CD69+ Tregs) displayed stronger ability to maintain immune tolerance. CD69+ Tregs expressed higher levels of suppression-associated markers such as CTLA-4, ICOS, CD38 and GITR, and secreted higher levels of IL-10 but not TGF-ß1. CD69+ Tregs from Il10+/+ rather than Il10-/- mice significantly inhibit the proliferation of CD4+ T cells. CD69 over-expression stimulated higher levels of IL-10 and c-Maf expression, which was compromised by silencing of STAT3 or STAT5. In addition, the direct interaction of STAT3 with the c-Maf promoter was detected in cells with CD69 over-expression. Moreover, adoptive transfer of CD69+ Tregs but not CD69-Tregs or CD69+ Tregs deficient in IL-10 dramatically prevented the development of inflammatory bowel disease (IBD) in mice. Taken together, CD69 is important to the suppressive function of Tregs by promoting IL-10 production. CD69+ Tregs have the potential to develop new therapeutic approach for autoimmune diseases like IBD.

CD8α+CD11c+ Extracellular Vesicles in the Lungs Control Immune Homeostasis of the Respiratory Tract via TGF-ß1 and IL-10.

The immune balance of the respiratory tract is strictly regulated. Extracellular vesicles (EVs) have been reported to participate in maintaining the immune balance in the intestinal tract, but whether they are involved in regulation of the immune balance in the respiratory tract has yet to be revealed. In this study, we found that physiological EVs from lungs of WT mice (L-EVs) could be isolated, which contained the immunosuppressive cytokines TGF-ß1 and IL-10. Among L-EV subsets, only the CD8α+CD11c+ EV subset was positive for TGF-ß1 and IL-10 and could inhibit CD4+ T cell proliferation via TGF-ß1 in vitro and relieve murine asthmatic symptoms. Mechanistically, L-EVs were effective at inhibiting OVA peptide-specific CD4+ T cell proliferation in a TGF-ß1- and IL-10-dependent manner. In addition, they could prevent CD4+ T cells from hilar lymph nodes from secreting IL-4, IL-9, and IL-17A via IL-10 ex vivo, suggesting inhibition of Th2, Th9, and Th17 cell responses. Altogether, our results indicate that EVs from the lungs are involved in control of the immune balance in the respiratory tract, which reveals a novel mechanism in the maintenance of respiratory tract immune homeostasis.

Prediction of the Iron-Based Polynuclear Magnetic Superhalogens with Pseudohalogen CN as Ligands.

To explore stable polynuclear magnetic superhalogens, we perform an unbiased structure search for polynuclear iron-based systems based on pseudohalogen ligand CN using the CALYPSO method in conjunction with density functional theory. The superhalogen properties, magnetic properties, and thermodynamic stabilities of neutral and anionic Fe2(CN)5 and Fe3(CN)7 clusters are investigated. The results show that both of the clusters have superhalogen properties due to their electron affinities (EAs) and that vertical detachment energies (VDEs) are significantly larger than those of the chlorine element and their ligand CN. The distribution of the extra electron analysis indicates that the extra electron is aggregated mainly into pseudohalogen ligand CN units in Fe2(CN)5¯ and Fe3(CN)7¯ cluster. These features contribute significantly to their high EA and VDE. Besides superhalogen properties, these two anionic clusters carry a large magnetic moment just like the Fe2F5¯ cluster. Additionally, the thermodynamic stabilities are also discussed by calculating the energy required to fragment the cluster into various smaller stable clusters. It is found that Fe(CN)2 is the most favorable fragmentation product for anionic Fe2(CN)5¯ and Fe3(CN)7¯ clusters, and both of the anions are less stable against ejection of Fe atoms than Fe(CN)n-x.

Investigation on the neutral and anionic BxAlyH2 (x + y = 7, 8, 9) clusters using density functional theory combined with photoelectron spectroscopy.

The structure and bonding nature of neutral and negatively charged BxAlyH2 (x + y = 7, 8, 9) clusters are investigated with the aid of previously published experimental photoelectron spectra combined with the present density functional theory calculations. The comparison between the experimental photoelectron spectra and theoretical simulated spectra helps to identify the ground state structures. The accuracy of the obtained ground state structures is further verified by calculating their adiabatic electron affinities and vertical detachment energies and comparing them against available experimental data. The results show that the structures of BxAlyH2 transform from three-dimensional to planar structures as the number of boron atoms increases. Moreover, boron atoms tend to bind together forming Bn units. The hydrogen atoms prefer to bind with boron atoms rather than aluminum atoms. The analyses of the molecular orbital on the ground state structures further support the abovementioned results.