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Alley, J.

Publications and source records attributed to Alley, J..

5 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↗

Preliminary attempt to inhibit proliferation of NUT carcinoma cell lines using antisense oligonucleotides targeting NUTM1

NUT carcinoma is an aggressive cancer driven by NUTM1 fusion proteins. This study evaluated antisense oligonucleotides (ASOs) targeting NUTM1 as a potential therapeutic approach. Three ASOs targeting NUTM1 and scrambled controls were tested at 10-50 nM doses in three NUT carcinoma cell lines (TC-797, 10-15, 14169) and one control line (293T). ASOs were delivered both gymnotically and using a transfection reagent. Cell viability was assessed at 48 and 72 hours using a luminescence-based assay. No ASOs showed selective inhibition of NUT carcinoma cell viability compared to controls across all conditions tested. Thus, this pilot study did not identify ASOs with activity against NUT carcinoma cells. However, it did establish preliminary protocols and generated data to inform future ASO optimization efforts targeting NUTM1 in NUT carcinoma. Further refinement of ASO design and delivery methods is needed to identify therapeutic candidates. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=135 SRC="FIGDIR/small/605673v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@de8a08org.highwire.dtl.DTLVardef@383db9org.highwire.dtl.DTLVardef@5c4500org.highwire.dtl.DTLVardef@1b6325f_HPS_FORMAT_FIGEXP M_FIG C_FIG HypothesisThis experiment was performed as a pilot experiment to generate data to inform future work, which should include formal hypothesis testing with a reduced number of conditions. The hypothesis of this pilot experiment was that one or more of the non-scrambled antisense oligonucleotides (ASOs) targeting NUTM1 will selectively decrease proliferation and/or viability of NUT carcinoma cells, indicated by a reduction in luminescence (as compared to treated non-NUT carcinoma and untreated NUT carcinoma control cells) using the CellTiter-Glo Luminescent Cell Viability Assay.

cancer biology↗

Structural basis for CCR6 modulation by allosteric antagonists

The CC chemokine receptor 6 (CCR6) is a potential target for chronic inflammatory diseases such as psoriasis and inflammatory bowel disease. Previously, we reported an active CCR6 structure in complex with its cognate chemokine CCL20, revealing the molecular basis of CCR6 activation mediated by CCL20. Here, we present two inactive CCR6 structures determined by cryo-EM in ternary complexes with different allosteric antagonists, CCR6/SQA1/OXM1 and CCR6/SQA1/OXM2. OXM1 and OXM2 are oxomorpholine (OXM) analogues which are highly selective for CCR6 and disrupt the molecular network critical for receptor activation by binding to an extracellular allosteric pocket within the transmembrane domain. A U-shaped conformation stabilized by intramolecular interactions was revealed by structural and NMR studies of active OXM analogues. SQA1 is a squaramide (SQA) derivative with close-in analogues that were previously reported to be antagonists of CCR6 and other chemokine receptors. Our structures reveal an intracellular pocket occupied by SQA1 that overlaps with the G protein binding site. In addition, SQA1 stabilizes a closed conformation of the intracellular pocket, a hallmark of the inactive state of GPCRs. Minimal communication was found between the two allosteric pockets. Overall, our work provides new evidence of the versatility of GPCR antagonism by small molecules, complementing previous knowledge on CCR6 activation, and sheds light on drug discovery approaches to target CCR6 for autoimmune disorders.

biochemistry↗

Integrated Metabolomic and Transcriptomic Profiling Reveals Novel Activation-Induced Metabolic Networks in Human T cells

The targeting of metabolic pathways is emerging as an exciting new approach for modulating immune cell function and polarization states. In this study, carbon tracing and systems biology approaches integrating metabolomic and transcriptomic profiling data were used to identify adaptations in human T cell metabolism important for fueling pro-inflammatory T cell function. Results of this study demonstrate that T cell receptor (TCR) stimulation leads to a significant increase in glucose and amino acid metabolism that trigger downstream biosynthetic processes. Specifically, increased expression of several enzymes such as CTPS1, IL4I1, and ASL results in the reprogramming of amino acid metabolism. Additionally, the strength of TCR signaling resulted in different metabolic enzymes utilized by T cells to facilitate similar biochemical endpoints. Furthermore, this study shows that cyclosporine represses the pathways involved in amino acid and glucose metabolism, providing novel insights on the immunosuppressive mechanisms of this drug. To explore the implications of the findings of this study in clinical settings, conventional immunosuppressants were tested in combination with drugs that target metabolic pathways. Results showed that such combinations increased efficacy of conventional immunosuppressants. Overall, the results of this study provide a comprehensive resource for identifying metabolic targets for novel combinatorial regimens in the treatment of intractable immune diseases.

immunology↗

Physical illness, social disadvantage, and risky sexual behavior in adolescence and young adulthood

This study investigated the influence of illness on sexual risk behavior in adolescence and the transition to adulthood, both directly and through moderation of the impact of social disadvantage. We hypothesized positive effects for social disadvantages and illness on sexual risk behavior, consistent with the development of faster life history strategies among young people facing greater life adversity. Using the first two waves of the National Longitudinal Study of Adolescent Health, we developed a mixed effects multinomial logistic regression model predicting sexual risk behavior in three comparisons, risky nonmonogamous sex vs. 1) safer nonmonogamous sex, 2) monogamous sex, and 3) abstinence, by social characteristics, illness, interactions thereof, and control covariates. Multiple imputation was used to address a modest amount of missing data. Subjects reporting higher levels of illness had lower odds of having safer nonmonogamous sex (OR = 0.84, p < .001), monogamous sex (OR = 0.82, p < .001), and abstinence (OR = 0.74, p < .001) vs. risky nonmonogamous sex, relative to individuals in better health. Illness significantly moderated the sex (OR = 0.88, p < .01), race/ethnicity (e.g., OR = 1.21, p < .001), and childhood SES (OR = 0.94; p < .01) effects for the abstinent vs. risky nonmonogamous sex comparison. Substantive findings were generally robust across waves and in various sensitivity analyses. These findings offer general support for the predictions of life history theory. Illness and various social disadvantages are associated with increased sexual risk behavior in adolescence and the transition to adulthood. Analyses indicate that the buffering effects of several protective social statuses against sexual risk-taking are substantially eroded by illness.

epidemiology↗