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Biology subjects

Thompson, M. A.

Publications and source records attributed to Thompson, M. A..

7 recordsLinked to original sources

Discovery of frameshift-associated TCRs following personalized neoantigen vaccination in a patient with osteosarcoma

Personalized antigen-directed immunotherapies, including personalized cancer vaccines, are emerging as promising therapeutic modalities for a range of cancer types. Immune monitoring can be used to evaluate the efficacy of a vaccine in stimulating the immune response pre- and post-vaccination; however, such approaches typically stop short of identifying which T cell receptors (TCRs) are functionally driving therapeutic responses. Here, we present a case report of immune monitoring and subsequent TCR discovery experiments following administration of personalized cancer vaccines in a patient with locally recurrent osteosarcoma. Whole PBMCs were stimulated with vaccine peptides (>16 AA) in vitro for 11 days, after which IFN{gamma} ELISPOT identified total T cell responses for 12 of 15 tested peptides post-vaccination. In vitro expanded samples were submitted for 10x single-cell TCR sequencing, from which 26 TCRs were chosen for generation of TCR-T cells based on clonal expansion and culture specificity. Of the generated TCR-T cells, 25 produced functional TCRs, 4 of which were specific to vaccine peptides. However, downstream testing revealed each was MHC class-II restricted. To address this, we repeated the in vitro stimulations with co-cultures of isolated CD8+ T cells with autologous dendritic cells, and cultures of whole PBMCs with anti-MHC class-II blocking antibody. These cultures yielded 10 additional TCRs, 2 of which were responsive to a vaccine peptide containing a MAP2 frameshift mutation. These findings demonstrate an effective approach for leveraging post-vaccination expanded antigen-specific T cell populations for discovery of novel T cell receptors for downstream cellular therapies.

immunology↗

Store-operated Ca2+ entry is involved in endothelium-to-mesenchymal transition in lung vascular endothelial cells

Endothelial-to-mesenchymal transition (EndMT) is a biological process that converts endothelial cells to mesenchymal cells with increased proliferative and migrative abilities. EndMT has been implicated in the development of pulmonary vascular remodeling in pulmonary arterial hypertension (PAH), a fatal and progressive lung vascular disease. Transforming growth factor {beta}1 (TGF-{beta}1), an inflammatory cytokine, is known to induce EndMT in many types of endothelial cells including lung vascular endothelial cells (LVEC). An increase in cytosolic free Ca2+ concentration ([Ca2+]cyt) is a major stimulus for cellular proliferation and phenotypic transition, but it is unknown whether Ca2+ signaling is involved in EndMT. In this study we tested the hypothesis that TGF-{beta}1-induced EndMT in human LVEC is Ca2+-dependent. Treatment of LVEC with TGF-{beta}1 for 5-7 days resulted in increase in SNAI1/2 expression, induction of EndMT, upregulation of STIM/Orai1 and enhancement of store-operated Ca2+ entry (SOCE). Removal (or chelation) of extracellular or intracellular Ca2+ with EGTA or BAPTA-AM respectively abolished EndMT in response to TGF-{beta}1. Moreover, EGTA diminished TGF-{beta}1-induced increase in SNAI in a dose-dependent manner. Knockdown of either STIM1 or Orai1 was sufficient to prevent TGF-{beta}-mediated increase in SNAI1/2 and EndMT, but did not rescue the continuous adherent junctions. Blockade of Orai1 channels by AnCoA4 inhibited TGF-{beta}-mediated EndMT and restored PECAM1-positive continuous adherent junctions. In conclusion, intracellular Ca2+ signaling plays a critical role in TGF-{beta}-associated EndMT through enhanced SOCE and STIM1-Orai1 interaction. Thus, targeting Ca2+ signaling pathways regulating EndMT may be a novel therapeutic approach to treat PAH and other forms of pre-capillary pulmonary hypertension. New & NoteworthyEndMT has been reported to contribute to the pathogenesis of PH. In this study we aimed to determine the role of Ca2+ signaling in the development of EndMT in human lung vascular endothelial cells. Our data suggest that TGF-{beta}1 requires store-operated Ca2+ entry through STIM1/Orai channels to induce SNAI-mediated EndMT. For the first time we demonstrated that TGF-{beta}1-induced EndMT is Ca2+-dependent event while inhibition of STIM1/Orai interaction attenuated EndMT in response to TGF-{beta}1.

cell biology↗

Olfactory chemosensation extends lifespan through TGF-β signaling and UPR activation

Animals rely on chemosensory cues to survive in pathogen-rich environments. In C. elegans, pathogenic bacteria are known to trigger aversive behaviors through neuronal perception, and to activate molecular defenses throughout the animal. This suggests that neurons may be able to coordinate the activation of organism-wide defensive responses upon pathogen perception. We find that exposure to volatile pathogen-associated compounds induces cell non-autonomous activation of the endoplasmic reticulum unfolded protein response (UPRER) in peripheral tissues following xbp-1 splicing in neurons. This odorant-induced UPRER activation is dependent upon transforming growth factor beta (TGF-{beta}) signaling and leads to extended lifespan and enhanced clearance of toxic proteins. Our data suggest that the cell non-autonomous UPRER rewires organismal proteostasis in response to pathogen detection, pre-empting the arrival of proteotoxic stress. Thus, chemosensation of particular odors may be a novel way to manipulate stress responses and longevity.

cell biology↗

Neuronal SKN-1B Modulates Nutritional Signalling Pathways and Mitochondrial Networks to Control Satiety

The feeling of hunger or satiety results from integration of the sensory nervous system with other physiological and metabolic cues. This regulates food intake, maintains homeostasis and prevents disease. In C. elegans, chemosensory neurons sense food and relay information to the rest of the animal via hormones to control food-related behaviour and physiology. Here we identify a new component of this system, SKN-1B which acts as a central food-responsive node, ultimately controlling satiety and metabolic homeostasis. SKN-1B, an ortholog of mammalian NF-E2 related transcription factors (Nrfs), acts in two hypothalamus-like ASI neurons to sense food, communicate nutritional status to the organism, and control satiety and exploratory behaviours. It achieves this by modulating endocrine signalling pathways (IIS and TGF-{beta}), and by promoting a robust mitochondrial network. Our data suggest a food-sensing and satiety role for mammalian Nrf proteins.

animal behavior and cognition↗

The TAT Protein Transduction Domain as an Intra-articular Drug-Delivery Technology

ObjectiveIntra-articular drug delivery holds great promise for the treatment of joint diseases such as osteoarthritis. The objective of this study was to evaluate the TAT peptide transduction domain (TAT-PTD) as a potential intra-articular drug delivery technology for synovial joints. DesignExperiments examined the ability of TAT conjugates to associate with primary chondrocytes and alter cellular function both in vitro and in vivo. Further experiments examined the ability of the TAT-PTD to bind to human osteoarthritic cartilage. ResultsThe results show that the TAT-PTD associates with chondrocytes, is capable of delivering siRNA for chondrocyte gene knockdown, and that the recombinant enzyme TAT-Cre is capable of inducing in vivo genetic recombination within the knee joint in a reporter mouse model. Lastly, binding studies show that osteoarthritic cartilage preferentially uptakes the TAT-PTD from solution. ConclusionsThe results suggest that the TAT-PTD is a promising delivery strategy for intra-articular therapeutics.

bioengineering↗

Thymic Stromal Lymphopoietin Promotes Proliferation and Contractility of Human Pulmonary Artery Smooth Muscle

Hypoxia is a well-recognized risk factor in several pulmonary vascular diseases including pulmonary hypertension (PH). Furthermore, hypoxia-associated inflammatory changes enhance the structural and functional changes in the pulmonary artery (PA) of PH patients. Understanding the mechanisms that link hypoxia and inflammation, particularly early in disease, is key to development of novel therapeutic avenues for PH. Thymic stromal lymphopoietin (TSLP) is an \"early\" inflammatory mediator thought to be critical in diseases such as asthma, chronic obstructive pulmonary disease and atopic dermatitis. TSLP has canonical effects on the immune system, but can also have non-canonical effects on resident lung cells, e.g. airway smooth muscle. Currently, the expression and role of TSLP in the PA is unknown. We hypothesized that locally-produced TSLP potentiates the effects of hypoxia in PA remodeling and contractility relevant to PH. Experiments in human PA endothelial cells (PAECs) and smooth muscle cells (PASMCs) found PAECs to be a larger source of TSLP which targets PASMCs to enhance intracellular Ca2+ responses to vasoconstrictor agonist as well as cell proliferation, acting via a number of signaling cascades including Stat3 and PI3/Akt. Hypoxia, acting via HIF1, enhanced PAEC production of TSLP, and promoted TSLP effects on PASMCs. Interestingly, TSLP per se enhance HIF1a. Overall, these novel data highlight a role for TSLP in hypoxia effects on the PA, and thus relevance for inflammation in PH.

physiology↗

Multiple Flagellin Proteins Have Distinct and Synergistic Roles in Agrobacterium tumefaciens Motility

Rotary flagella propel bacteria through liquid and across semi-solid environments. Flagella are composed of the basal body that constitutes the motor for rotation, the curved hook that connects to the basal body, and the flagellar filament that propels the cell. Flagellar filaments can be comprised of a single flagellin protein such as in Escherichia coli or with multiple flagellins such is in Agrobacterium tumefaciens. The four distinct flagellins FlaA, FlaB, FlaC and FlaD produced by wild type A. tumefaciens, are not redundant in function, but have specific properties. FlaA and FlaB are much more abundant than FlaC and FlaD and are readily observable in mature flagellar filaments, when either FlaA or FlaB is fluorescently labeled. Cells having FlaA with any one of the other three flagellins can generate functional filaments and thus are motile, but FlaA alone cannot constitute a functional filament. In flaA mutants that manifest swimming deficiencies, there are multiple ways by which these mutations can be phenotypically suppressed. These suppressor mutations primarily occur within or upstream of the flaB flagellin gene or in the transcriptional factor sciP regulating flagellar expression. The helical conformation of the flagellar filament appears to require a key asparagine residue present in FlaA and absent in other flagellins. However, FlaB can be spontaneously mutated to render helical flagella in absence of FlaA, reflecting their overall similarity and perhaps the subtle differences in the specific functions they have evolved to fulfill.\n\nImportanceFlagellins are abundant bacterial proteins comprising the flagellar filaments that propel bacterial movement. Several members of the Alphaproteobacterial group express multiple flagellins, in contrast to model systems such as Escherichia coli that has only one flagellin protein. The plant pathogen Agrobacterium tumefaciens has four flagellins, the abundant and readily detected FlaA and FlaB, and lower levels of FlaC and FlaD. Mutational analysis reveals that FlaA requires at least one of the other flagellins to function - flaA mutants produce non-helical flagella and cannot swim efficiently. Suppressor mutations can rescue this swimming defect through mutations in the remaining flagellins, including structural changes imparting flagellar helical shape, and putative regulators. Our findings shed light on how multiple flagellins contribute to motility.

microbiology↗