We report a unique approach in which living cells direct their integration into 3D solid-state nanostructures. Yeast cells deposited on a weakly condensed lipid/silica thin film mesophase actively reconstruct the surface to create a fully 3D bio/nano interface, composed of localized lipid bilayers enveloped by a lipid/silica mesophase, through a self-catalyzed silica condensation process. Remarkably, this integration process selects exclusively for living cells over the corresponding apoptotic cells (those undergoing programmed cell death), via the development of a pH gradient, which catalyzes silica deposition and the formation of a coherent interface between the cell and surrounding silica matrix. Added long-chain lipids or auxiliary nanocomponents are localized within the pH gradient, allowing the development of complex active and accessible bio/nano interfaces not achievable by other synthetic methods. Overall, this approach provides the first demonstration of active cell-directed integration into a nominally solid-state three-dimensional architecture. It promises a new means to integrate "bio" with "nano" into platforms useful to study and manipulate cellular behavior at the individual cell level and to interface living organisms with electronics, photonics, and fluidics.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1021/nn101793u | DOI Listing |
Nat Rev Rheumatol
January 2025
Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA.
Classic regulatory T (T) cells expressing CD4 and the hallmark transcription factor FOXP3 are integral to the prevention of multi-system autoimmunity. However, immune-mediated arthritis is often associated with increased numbers of T cells in the inflamed joints. To understand these seemingly conflicting observations, which we collectively describe as 'the T paradox', we provide an overview of T cell biology with a focus on T cell heterogeneity, function and dysfunction in arthritis.
View Article and Find Full Text PDFbioRxiv
October 2024
Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Development of safe and effective subunit vaccines for controlling African Swine Fever Virus (ASFV) infection has been hampered by a lack of protective viral antigens, complex virion structures, and multiple mechanisms of infection. Here, we selected ASFV antigens based on their localization on the virion, known functions, and homologies to the subunits of the protective vaccinia virus vaccine. We also engineered viral capsid proteins for inducing optimal antibody responses and designed T cell-directed antigen for inducing broad and robust cellular immunity.
View Article and Find Full Text PDFMol Cancer Ther
December 2024
Case Comprehensive Cancer Center, School of Medicine, Case Western Reserve University, Cleveland, Ohio.
Proteasomes generate antigenic peptides that are presented on the tumor surface to cytotoxic T-lymphocytes. Immunoproteasomes are highly specialized proteasome variants that are expressed at higher levels in antigen-presenting cells and contain replacements of the three constitutive proteasome catalytic subunits to generate peptides with a hydrophobic C-terminus that fit within the groove of MHC class I (MHC-I) molecules. A hallmark of cancer is the ability to evade immunosurveillance by disrupting the antigen presentation machinery and downregulating MHC-I antigen presentation.
View Article and Find Full Text PDFBlood
July 2024
Division of Pediatric Hematology-Oncology, Boston Children's Hospital, Boston, MA.
Chimeric antigen receptor (CAR) T cells hold promise as a therapy for B-cell-derived malignancies, and despite their impressive initial response rates, a significant proportion of patients ultimately experience relapse. Although recent studies have explored the mechanisms of in vivo CAR T-cell function, little is understood about the activation of surrounding CARneg bystander T cells and their potential to enhance tumor responses. We performed single-cell RNA sequencing on nonhuman primate (NHP) and patient-derived T cells to identify the phenotypic and transcriptomic hallmarks of bystander activation of CARneg T cells following B-cell-targeted CAR T-cell therapy.
View Article and Find Full Text PDFImmunol Rev
May 2024
Immunology Program, Memorial Sloan Kettering Cancer Center, New York City, New York, USA.
Cancer progression can be restrained by tumor-infiltrating lymphocytes in a process termed cancer immunosurveillance. Based on how lymphocytes are activated and recruited to the tumor tissue, cancer immunity is either pre-wired, in which innate lymphocytes and innate-like T cells are directly recruited to and activated in tumors following their differentiation in primary lymphoid organs; or priming-dependent, in which conventional adaptive T cells are first primed by cognate antigens in secondary lymphoid organs before homing to and reactivated in tumors. While priming-dependent cancer immunity has been a focus of cancer immunology research for decades, in part due to historical preconception of cancer theory and tumor model choice as well as clinical success of conventional adaptive T cell-directed therapeutic programs, recent studies have revealed that pre-wired cancer immunity mediated by tissue-resident type 1 innate lymphoid cells (ILC1s) and killer innate-like T cells (ILTCKs) is an integral component of the cancer immunosurveillance process.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!