Carrier-selective contacts have become a prominent path forward toward efficient crystalline silicon (c-Si) photovoltaics. Among the proposed contacting materials, organic materials may offer simplified and low-cost processing compared with typical vacuum deposition techniques. Here, branched polyethylenimine (b-PEI) is presented as an electron-transport layer (ETL) for c-Si solar cells. The incorporation of a b-PEI interlayer between c-Si(n) and Al leads to a low contact resistivity of 24 mω cm2. A silicon heterojunction solar cell integrated with b-PEI is demonstrated achieving a power conversion efficiency of 19.4%, which improves the benchmark efficiency of a c-Si solar cell with an organic ETL. This electron selectivity of b-PEI is attributed to its Lewis basicity, i.e., electron-donating ability, promoting favorable band bending at the c-Si surface for electron transport. Moreover, several other Lewis base polymers perform as efficient ETLs in organic/c-Si hybrid devices, indicating Lewis basicity could be a guideline for future organic ETL design.

The global photovoltaic (PV) market is dominated by crystalline silicon (c-Si) based technologies with heavily doped, directly metallized contacts. Recombination of photo-generated electrons and holes at the contact regions is increasingly constraining the power conversion efficiencies of these devices as other performance-limiting energy losses are overcome. To move forward, c-Si PV technologies must implement alternative contacting approaches. Passivating contacts, which incorporate thin films within the contact structure that simultaneously supress recombination and promote charge-carrier selectivity, are a promising next step for the mainstream c-Si PV industry. In this work, we review the fundamental physical processes governing contact formation in c-Si. In doing so we identify the role passivating contacts play in increasing c-Si solar cell efficiencies beyond the limitations imposed by heavy doping and direct metallization. Strategies towards the implementation of passivating contacts in industrial environments are discussed.

The focus of this work is on the nano-scale characterization of transition metal oxides employed as carrier selective contacts in crystalline silicon (c-Si) solar cells using crosssectional transmission electron microscopy (TEM). Both electronselective (titanium dioxide, TiO 2 ) and hole-selective (molybdenum oxide, MoO x ; tungsten oxide, WO x textbf) contacts were investigated. High-resolution TEM (HRTEM) images were obtained with a FEI Tecnai F30 TEM.

The median overall survival for children with diffuse intrinsic pontine glioma (DIPG) is less than one year. The majority of diffuse midline gliomas, including more than 70% of DIPGs, harbor an amino acid substitution from lysine (K) to methionine (M) at position 27 of histone 3 variant 3 (H3.3). From a CD8⁺ T cell clone established by stimulation of HLA-A2⁺ CD8⁺ T cells with synthetic peptide encompassing the H3.3K27M mutation, complementary DNA for T cell receptor (TCR) α- and β-chains were cloned into a retroviral vector. TCR-transduced HLA-A2⁺ T cells efficiently killed HLA-A2⁺H3.3K27M⁺ glioma cells in an antigen- and HLA-specific manner. Adoptive transfer of TCR-transduced T cells significantly suppressed the progression of glioma xenografts in mice. Alanine-scanning assays suggested the absence of known human proteins sharing the key amino acid residues required for recognition by the TCR, suggesting that the TCR could be safely used in patients. These data provide us with a strong basis for developing T cell-based therapy targeting this shared neoepitope.

TCR-signaling strength generally correlates with peptide-MHC binding affinity; however, exceptions exist. We find high-affinity, yet non-stimulatory, interactions occur with high frequency in the human T cell repertoire. Here, we studied human TCRs that are refractory to activation by pMHC ligands despite robust binding. Analysis of 3D affinity, 2D dwell time, and crystal structures of stimulatory versus non-stimulatory TCR-pMHC interactions failed to account for their different signaling outcomes. Using yeast pMHC display, we identified peptide agonists of a formerly non-responsive TCR. Single-molecule force measurements demonstrated the emergence of catch bonds in the activating TCR-pMHC interactions, correlating with exclusion of CD45 from the TCR-APC contact site. Molecular dynamics simulations of TCR-pMHC disengagement distinguished agonist from non-agonist ligands based on the acquisition of catch bonds within the TCR-pMHC interface. The isolation of catch bonds as a parameter mediating the coupling of TCR binding and signaling has important implications for TCR and antigen engineering for immunotherapy.