Biology subjects

Sinclair, L. V.

Publications and source records attributed to Sinclair, L. V..

At least 19 recordsLinked to original sources

bioRxiv2026

Lysosomal adaptation to extracellular acidity compromises CD8+ T cell cytotoxicity

Extracellular acidosis is a hallmark of aggressive tumors and suppresses cytotoxic-T lymphocyte (CTL)-mediated killing, but how sustained acid exposure reshapes T cell cytotoxicity is poorly understood. Here we show that chronic acidosis drives lysosomal remodeling in human CD8+ T cells, converting the lysosome into a proton sink whose adaptation ultimately impairs killing by depleting the intracellular granzyme B reservoir through constitutive vesicle release. Quantitative proteomics of CD8+ T cells cultured at pH 6.5 identified lysosomes as the dominant target of acid-driven remodeling: CTLs upregulated the V1 sector of the vacuolar H+-ATPase and hyper-acidified the lysosomal lumen. The remodeled compartment accumulated lysosomal membrane proteins (LAMP1, LAMP2, CD63, CD68) post-transcriptionally, acquired higher cathepsin abundance and increased proteolytic activity. Chronic acidity also enlarged endoplasmic reticulum (ER) and lysosomal Ca2+ stores without altering cytosolic Ca2+, and drives constitutive, Ca2+-dependent release of LAMP1+ lysosome-derived vesicles, which drains the intracellular reservoir of granzyme B, contributing to reduced CTL activity. These findings establish lysosomal adaptation as a cost of surviving extracellular acidosis and identify lysosomal hydrolase activity as a possible target for improving CTL function in the acidic tumor environment.

immunology↗

bioRxiv2026

Physiological fatty acid uptake reveals spatial and systemic constraints on nutrient accessibility in vivo

Immune cells rely on exogenous fatty acids (FA) for membrane synthesis, bioenergetics and signalling, yet current approaches cannot accurately quantify physiological FA uptake in vivo. Here, we use cyclopropene-tagged fatty acids (cpFA) that, unlike existing FA-uptake tools, are taken up by physiologically relevant mechanisms. We measure FA uptake at single-cell resolution in vivo and uncover a previously unappreciated distinction between nutrient uptake capacity and nutrient accessibility. Although arachidonic acid exhibits the highest uptake capacity ex vivo across immune populations, it displays limited tissue accessibility in vivo, whereas palmitate is broadly accessible. In vivo nutrient-uptake measurements reveal that tissue architecture shapes nutrient accessibility, with spatial constraints in the spleen and exclusion of circulating FA, but not amino acids, from the thymus. Together, these findings identify nutrient accessibility as a distinct layer of metabolic regulation and reveal that immune-cell metabolism is shaped by spatial and systemic constraints on nutrient access HighlightsO_LINutrient accessibility is a distinct layer of metabolic regulation C_LIO_LIPhysiological FA uptake differs from ex vivo uptake capacity C_LIO_LISpatial and systemic factors govern fatty-acid accessibility C_LIO_LITissue context shapes immune-cell metabolism in vivo C_LI In briefUsing bioorthogonal FA to quantify physiological nutrient uptake in vivo, Wang et al. show that nutrient accessibility is distinct from nutrient uptake capacity. Tissue architecture and systemic FA distribution create spatial constraints on nutrient access, revealing an underappreciated layer of metabolic regulation in immune cells.

immunology↗

bioRxiv2026

Tumour microenvironments impose translational repression that limits natural killer cell persistence

Natural killer (NK) cells infiltrate many solid tumours, yet the mechanisms that determine their functional heterogeneity across tumour types remain poorly understood. Differences in tumour immunogenicity, inhibitory signalling, and nutrient availability have all been implicated, but unifying explanations are lacking. Here, we compared four syngeneic tumour models implanted at identical anatomical sites to isolate tumour-intrinsic effects on NK-cell fate. Tumour-infiltrating NK cells displayed striking tumour-specific differences in cytokine production, cytotoxic protein expression, and persistence. These differences were not explained by cytokine availability or global features of the tumour metabolic environment. Instead, quantitative proteomics and time-resolved in vivo labelling revealed that NK cells enter tumours in a functionally competent state but rapidly diverge thereafter. In suppressive tumour microenvironments, NK cells undergo early mitochondrial loss, translational repression, and impaired proteostatic responses, accompanied by increased apoptotic priming. These defects result in reduced effector function and failure of intratumoural persistence despite preserved recruitment. In contrast, permissive tumours sustain NK-cell translational capacity, cytokine responsiveness, and long-term residency. Together, these findings identify disruption of translational and mitochondrial homeostasis as a central mechanism limiting NK-cell persistence in solid tumours. This work establishes early tumour-induced defects in protein synthesis and cellular fitness as key constraints on durable NK-cell immunity and provides a framework for restoring effective innate anti-tumour responses.

immunology↗

bioRxiv2026

Asparagine availability differentially regulates early vs late CD4+ and CD8+ T cell activation, metabolism and autophagy

T cell activation is associated with, and dependent upon, the upregulation of amino acid uptake from the extracellular environment. Uptake of the non-essential amino acid asparagine (Asn) is mediated via amino transporters such as Slc1a5 whilst Asn can be synthesized within cells that express asparagine synthetase (ASNS). Previous work demonstrated that initial activation of CD8+ T cells is perturbed in the absence of Asn, whereas effector cytotoxic T cells cells upregulate ASNS and lose their dependence on Asn uptake. By contrast, less is known of the role of Asn uptake and ASNS in CD4+ T cell responses. Here we demonstrate that CD4+ T cells are more reliant than CD8+ T cells on Asn uptake for initial activation, differentiation, metabolic reprogramming and regulation of autophagy. These phenotypes are associated with enhanced expression of ASNS in CD8+ as compared to CD4+ effector T cells.

immunology↗

bioRxiv2025

A Novel Cyclopropenyl Fatty Acid Library Reveals Tissue-Specific Preferences for Regulatory T Cell Uptake Through Click-Chemistry

The activation of T-cells is heavily shaped by the nutrients that are available during activation. Fatty acids can have highly pleiotropic effects in this process. On the one hand, they are essential for driving T-cell activation, yet on the other hand they can affect curtailed T-cell activation. These differences are likely dependent on the nature and absolute uptake of the fatty acids. Quantifying the uptake of specific FAs by individual cells and studying the effect on the phenotype of the cell is currently not possible with existing tools. Here we therefore use the live-cell compatible Inverse Electron-Demand Diels-Alder reaction combined with the synthesis of saturated, unsaturated and polyunsaturated fatty acids carrying the 1-carbon cyclopropene click group. Single cell uptake studies of these various clickable FAs in primary immune cell mixtures show highly divergent uptake behaviour between different immune cells, with polyunsaturated fatty acids markedly preferred by all immune cells tested.

immunology↗

bioRxiv2025

ABHD11 inhibition drives sterol metabolism to modulate T cell effector function and alleviate autoimmunity

Chronic inflammation in autoimmunity is driven by T cell hyperactivation. This unregulated response to self is fuelled by heightened metabolic programmes, which offers a promising new direction to uncover novel treatment strategies. /{beta}-hydrolase domain-containing protein 11 (ABHD11) is a mitochondrial hydrolase that maintains the catalytic function of -ketoglutarate dehydrogenase (-KGDH), and its expression in CD4+ T cells has been linked to remission status in rheumatoid arthritis (RA). However, the importance of ABHD11 in regulating T cell metabolism and function - and thus, the downstream implication for autoimmunity - is yet to be explored. Here, we show that pharmacological inhibition of ABHD11 dampens cytokine production by human and mouse T cells. Mechanistically, the anti-inflammatory effects of ABHD11 inhibition are attributed to increased 24,25-epoxycholesterol (24,25-EC) biosynthesis and subsequent liver X receptor (LXR) activation, which arise from a compromised TCA cycle. The impaired cytokine profile established by ABHD11 inhibition is extended to two patient cohorts of autoimmunity. Importantly, using a murine model of accelerated type 1 diabetes (T1D), we show that targeting ABHD11 suppresses cytokine production in antigen-specific T cells and delays the onset of diabetes in vivo. Collectively, our work provides pre-clinical evidence that ABHD11 is an encouraging drug target in T cell-mediated autoimmunity. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/643996v1_ufig1.gif" ALT="Figure 1"> View larger version (59K): org.highwire.dtl.DTLVardef@bb3fcborg.highwire.dtl.DTLVardef@1594fc8org.highwire.dtl.DTLVardef@84e078org.highwire.dtl.DTLVardef@1ad023e_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

bioRxiv2024

A proteomic map of B cell activation and its shaping by mTORC1, MYC and iron

Using high resolution quantitative mass spectrometry, we have explored how immune activation and the metabolic checkpoint kinase mTORC1 (mammalian target of rapamycin complex 1) regulate the proteome of B lymphocytes. B cell activation via the B cell receptor, CD40 and the IL4 receptor induced considerable re-modelling of the B cell protein landscape, with a 5-fold increase in total cellular protein mass within 24 hours of activation. Analysis of copy numbers per cell of >7,500 proteins revealed increases in the metabolic machinery that supports B cell activation and nutrient and amino acid transporters that fuel B cell biosynthetic capacity. Comparison of T cell-dependent versus T cell-independent B cell stimulation along with an analysis of the synergistic effects of stimuli, identified shared and unique impacts of stimuli and highlighted the drivers of B cell proteome remodelling. In addition, we reveal that mTORC1 controls activation-induced B cell growth and inhibiting mTORC1 impairs the expression of amino acid transporters that fuel B cell protein production. We also show that mTORC1 activity regulates the expression of the transcription factor MYC and the transferrin receptor CD71. Blocking MYC activity phenocopied mTORC1 inhibition in many ways including impaired CD71 expression, while limiting iron availability during B cell activation impaired B cell growth and protein synthesis. This work provides a detailed map of naive and immune activated B cell proteomes and a greater understanding of the cellular machinery that directs B cell phenotypes. This work also provides new insights into the role of mTORC1, MYC and iron in regulating activation-induced proteome remodelling and protein production in B cells.

immunology↗

bioRxiv2024

LPS stimulates dynamic changes in B cell metabolism to promote proliferation

Naive B cells exit quiescence and enter a proliferative state upon activation, ultimately differentiating into antibody-secreting or memory B cells. Toll-like receptor (TLR) ligands, such as lipopolysaccharide (LPS), can serve as physiological stimuli to initiate this transition. Using quantitative proteomics, we show that TLR4 engagement induces metabolic reprogramming in murine B cells, increasing the expression of amino acid transporters and cholesterol biosynthetic enzymes. The amino acid transporter SLC7A5 is markedly upregulated following LPS stimulation, and conditional deletion of Slc7a5 impairs B cell proliferation, underscoring its essential role in B cell activation. LPS also elevates intracellular cholesterol levels, and inhibition of the rate-limiting enzyme HMG-CoA reductase blocks proliferation. This effect was mediated by a dual requirement for cholesterol metabolism and protein prenylation downstream of HMG-CoA reductase. Notably, this was not unique to TLR4 signalling but is also observed in B cells activated via TLR7, TLR9, CD40, or the B cell receptor. Together, these findings reveal that metabolic rewiring, including amino acid uptake and cholesterol metabolism, is an essential feature of B cell activation and proliferation.

immunology↗

bioRxiv2024

Autophagy repression by antigen and cytokines shapes mitochondrial, migration and effector machinery in CD8 T cells.

Autophagy is important for CD8 T-cells but autophagy timing, triggers and targets are poorly defined. Herein, we show naive CD8-T cells have high autophagic flux and identify an autophagy checkpoint whereby antigen receptor engagement represses autophagy by regulating amino acid transporter expression and intracellular amino acid delivery. Effector cytotoxic T cells with high levels of amino acid transporters driven by proinflammatory cytokines have low autophagic flux but rapidly reinduce autophagy when amino acid restricted. A census of proteins degraded and fuelled by autophagy shows how autophagy shapes CD8-T cell proteomes. In cytotoxic T-cells, dominant autophagy substrates include cytolytic effector molecules, amino acid and glucose transporters. In naive T-cells mitophagy dominates and selective mitochondrial pruning supports the expression of molecules that coordinate T-cell migration and survival. Autophagy thus differentially prunes naive and effector T-cell proteomes and is dynamically repressed by antigen receptors and inflammatory cytokines to shape T-cell differentiation.

immunology↗

bioRxiv2024

Iron deficiency causes aspartate-sensitive metabolic and proliferative dysfunction in CD8+ T cells

Iron is an irreplaceable co-factor for metabolism. Iron deficiency affects >1 billion people, causing symptoms including anaemia and impaired immunity. Nevertheless, precisely how iron deprivation impacts immune cell function remains poorly characterised. We therefore interrogated how physiologically low iron availability affected activated CD8+ T cell metabolism and function, using multi-omic and metabolic labelling approaches. Iron limitation profoundly stalled proliferation without influencing cell viability, altered histone methylation status and disrupted mitochondrial membrane potential. Consistently, metabolism of glucose and glutamine in the TCA cycle was limited, indeed TCA cycle activity was partially reversed to a reductive trajectory. Previous studies have shown mitochondria-derived aspartate is crucial for proliferation of transformed cells. Surprisingly, we found aspartate was increased in stalled iron deficient CD8+ T-cells, but was not utilised cytosolically for nucleotide synthesis, likely due to trapping within depolarised mitochondria. Conversely, exogenous aspartate, which directly accesses the cytosol, markedly rescued the clonal expansion of even severely iron-deficient CD8+ T-cells. Overall, iron scarcity creates a mitochondrial-located metabolic bottleneck impairing T-cells, which can be bypassed by resupplying inhibited biochemical processes with aspartate. These findings reveal molecular consequences of iron deficiency for CD8+ T cell function, providing mechanistic insight into the basis for immune impairment during iron deficiency.

immunology↗

bioRxiv2024

Iron deficiency in people with obesity drives defective natural killer cell mitochondrial fitness and function

Natural killer (NK) cells are a population of innate effector lymphocytes, involved in host-defences against viral infections and cancer. Upon activation, NK cells can produce a milieu of cytotoxic molecules and cytokines, which can directly target infected and transformed cells, but also amplify an immune response. Metabolic rewiring underpins NK cell effector functionality, providing the required signals, energy and biointermediates to support their immune responses. Obesity is associated with significant defects in the functionality of human NK cells, especially in the periphery. Dysregulated cellular metabolism has been demonstrated to be a major mechanistic driver of the reported defects. However, how obesity links to defective NK cell metabolism and functionality remains unclear. Iron deficiency is a common co-morbidity in people living with obesity (PWO). Recent studies have highlighted the importance for iron in host immunity, with murine models of iron deficiency resulting in defective cellular metabolism and function. We hypothesized that obesity-driven iron deficiency might underpin the reported defects in NK cells. Our data demonstrates that in response to cytokine stimulation, healthy human NK cells utilize iron to support their metabolic activity and cytokine responses. In a cohort of PWO, we demonstrate alterations in NK cell metabolism, mitochondrial fitness and cytokine production. Furthermore, upon stratification into PWO with normal iron status versus low iron status, we show the observed obesity-related defects in NK cell metabolism, mitochondrial fitness and cytokine production are concentrated in the PWO with low-iron status. Collectively, our data highlights the importance of iron for human NK cell responses and provides evidence that obesity-driven defects in NK cell metabolism and function are linked in part to altered iron availability.

immunology↗

bioRxiv2022

Glycogen-fuelled metabolism supports rapid Mucosal Associated Invariant T cell responses

Mucosal Associated Invariant T (MAIT) cells are a subset of unconventional T cells, which recognise a limited repertoire of ligands presented by the MHC class I-like molecule MR1. In addition to their key role in host protection against bacterial and viral pathogens, MAIT cells are emerging as potent anti-cancer effectors. With their abundance in human, unrestricted properties and rapid effector functions, MAIT cells are emerging as attractive candidates for cancer-immunotherapy. In the current study, we demonstrate that MAIT cells are potent anti-tumour cells, rapidly degranulating and inducing target cell death. Previous work from our group and others has highlighted glucose metabolism as a critical process for MAIT cell cytokine responses at 18 hours. However, the metabolic processes supporting rapid MAIT cell anti-tumour responses are currently unknown. Here, we show that glucose metabolism is dispensable for both MAIT cell cytotoxicity and early (<3 hours) cytokine production, as is oxidative phosphorylation. We show for the first time that MAIT cells have the machinery required to make and metabolize glycogen, and demonstrate that MAIT cell cytotoxicity and rapid cytokine responses are dependent on glycogen metabolism. In summary, we show for the first time that glycogen-fuelled metabolism supports rapid MAIT cell effector functions (cytotoxicity and cytokine production) which may have implications in their use as an immunotherapeutic agent.

immunology↗

bioRxiv2022

QUAS-R: Glutamine (Q) Uptake Assay with Single cell Resolution reveals metabolic heterogeneity with immune populations.

System level analysis of single cell data is rapidly transforming the field of immunometabolism. However, metabolic profiling of single cells and small populations by flow and mass cytometry is extremely limited by the availability of specific reagents such as antibodies and fluorescently nutrient analogues. Given the competitive demand for nutrients in pathogenic microenvironments including sites of infection, tumours and autoinflammation, there is a need to understand how and when immune cells access these nutrients. Fluorescent-tagging of nutrients is one approach to study nutrient transport but is extremely limited in its usefulness as tagging usually changes the transport characteristics and transporter specificity of the nutrient. Herein, we developed a completely new approach for single cell analysis of nutrient uptake where a fluorophore is attached to a functionalized amino acid after it has been transported across the plasma membrane and is within the cell. This in-cell biorthogonal labelling ensures that bona fide transport has been measured. System ASC transporter SLC1A5/ASCT2 transports multiple amino acids, most notably the crucial fuel glutamine, and has essential roles in supporting immune metabolism, signalling and function. This flow cytometry assay allows for rapid, sensitive, and quantitative measurement of SLC1A5-mediated uptake, which we used to interrogate the transport capacity of the complex immune subpopulations within the thymus, at a single cell resolution previously "unreachable". Taken together, our findings provide an easy procedure to assess which cells support their function via SLC1A5 mediated uptake of amino acids in a sensitive single cell assay. This assay is a significant addition to the single-cell metabolic toolbox required to decode the metabolic landscape of complex immune microenvironments.

immunology↗

bioRxiv2022

The Immunological Proteome Resource

The Immunological Proteome Resource (ImmPRes; http://immpres.co.uk/) is an open access public resource integrating proteomic data generated by large-scale mass-spectrometry analysis of murine hematopoietic populations. The initial focus is T lymphocytes and how their proteomes are shaped by immune activation, environment, and intracellular signalling pathways with an aim to expand it to B cells and innate immune cells. It is a multidisciplinary effort between immunology and mass spectrometry-based labs with the objective to help define an in-depth high-quality map of immune cell proteomes. Maintaining data reproducibility and integrity are a priority within the resource, thus there is an in-depth protocols section explaining in detail the sample processing and the mass spectrometry-based analysis. ImmPRes provides open access to proteomic datasets covering a wide range of murine leukocyte populations with analysis of copy numbers per cell of > 10,000 proteins, enabling new understanding of lymphocyte phenotypes. All data is accessible via a simple graphical interface that supports easy interrogation of the data and options to download data summaries and raw data files.

immunology↗

bioRxiv2022

Human Mucosal Associated Invariant T cell proliferation is dependent on a MYC-SLC7A5-Glycolysis metabolic axis

Mucosal Associated Invariant T (MAIT) cells are an abundant population of innate T cells which recognise bacterial ligands presented by the MHC class-I like molecule MR1. MAIT cells play a key role in host protection against bacterial and viral pathogens. Upon activation MAIT cells undergo proliferative expansion and increased production of effector molecules such as cytokines. The molecular and metabolic mechanisms controlling MAIT cell effector functions are still emerging. In this study, we found that expression of the key metabolism regulator and transcription factor MYC is upregulated in MAIT cells upon immune stimulation. Using quantitative mass spectrometry, we identified the activation of two MYC controlled metabolic pathways; amino acid transport and glycolysis, both of which are critical for MAIT cell proliferation. Finally, we show that MYC expression in response to immune activation is diminished in MAIT cells isolated from people with obesity, resulting in defective MAIT cell proliferation and functional responses. Collectively our data details for the first time the importance of MYC regulated metabolism for MAIT cell proliferation, and provides additional insight into the molecular defects underpinning functional failings of MAIT cells in obesity. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=175 SRC="FIGDIR/small/476571v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@29d1bforg.highwire.dtl.DTLVardef@1896004org.highwire.dtl.DTLVardef@1febefdorg.highwire.dtl.DTLVardef@1ad0754_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

bioRxiv2021

A quantitative comparison of human embryonic and induced stem cell proteomes

Human induced pluripotent stem cells (hiPSCs) have great potential to be used as alternatives to embryonic stem cells (hESCs) in regenerative medicine and disease modelling, thereby avoiding many of the ethical issues arising from the use of embryo-derived cells. However, despite clear similarities between the two cell types, it is likely they are not identical. In this study, we characterise the proteomes of multiple hiPSC and hESC lines derived from independent donors. We find that while hESCs and hiPSCs express a near identical set of proteins, they show consistent quantitative differences in the expression levels of a wide subset of proteins. hiPSCs have increased total protein content, while maintaining a comparable cell cycle profile to hESCs. The proteomic data show hiPSCs have significantly increased abundance of vital cytoplasmic and mitochondrial proteins required to sustain high growth rates, including nutrient transporters and metabolic proteins, which correlated with phenotypic differences between hiPSCs and hESCs. Thus, higher levels of glutamine transporters correlated with increased glutamine uptake, while higher levels of proteins involved in lipid synthesis correlated with increased lipid droplet formation. Some of the biggest metabolic changes were seen in proteins involved in mitochondrial metabolism, with corresponding enhanced mitochondrial potential, shown experimentally using high-resolution respirometry. hiPSCs also produced higher levels of secreted proteins, including ECM components and growth factors, some with known tumorigenic properties, as well as proteins involved in the inhibition of the immune system. Our data indicate that reprogramming of human fibroblasts to iPSCs effectively restores protein expression in cell nuclei to a state comparable to hESCs, but does not similarly restore the profile of cytoplasmic and mitochondrial proteins, with consequences for cell phenotypes affecting growth and metabolism. The data improve understanding of the molecular differences between induced and embryonic stem cells, with implications for potential risks and benefits for their use in future disease modelling and therapeutic applications.

biochemistry↗

bioRxiv2020

Large Neutral Amino acid uptake and mTOR activation within CD4+ T cells coordinate Type 2 immunity and host resistance to Trichuris muris

Trichuris trichiura (whipworm) is a gastrointestinal nematode that infects approximately 465 million people worldwide. T. muris is used as a tractable model for the human whipworm. In wild type mice, infection with a high dose of T. muris eggs leads to worm expulsion, which is dependent on a CD4+Th2 response and interleukin (IL-)13 production. It is known that T cells up-regulate glycolysis and uptake of substrates upon activation. The amino acid transporter SLC7A5 has been shown necessary for activation of mTORC1, a nutrient/energy/redox sensor critical for T cell differentiation into effector cells. We found that at the peak of the immune response to T. muris, mice lacking SLC7A5 in CD4+T cells have delayed worm expulsion, lower levels of IL-13, reduced pmTOR and glycolytic rates. However, at later stages of infection IL-13 levels partially recovered alongside resistance. The critical role of CD4+T cell metabolism per se and down-stream mTOR in CD4+T cells in resistance was shown in mice lacking mTOR in CD4+T cells, that failed to expel a high dose of parasites and developed chronic infection. Our study shows that mTOR is essential for effective functioning of T cells during whipworm infection and that deletion of Slc7a5 significantly delays worm clearance.

immunology↗

bioRxiv2019

Quantitative analysis of how Myc controls T cell proteomes and metabolic pathways during T cell activation

T cell expansion and differentiation are critically dependent on the transcription factor c-Myc (Myc). Herein we use quantitative mass-spectrometry to reveal how Myc controls antigen receptor driven cell growth and proteome restructuring in T cells. Analysis of copy numbers per cell of >7000 proteins provides new understanding of the selective role of Myc in controlling the protein machinery that govern T cell fate. The data identify both Myc dependent and independent metabolic processes in immune activated T cells. We uncover that a primary function of Myc is to control expression of multiple amino acid transporters and that loss of a single Myc-controlled amino acid transporter effectively phenocopies the impact of Myc deletion. This study provides a comprehensive map of how Myc selectively shapes T cell phenotypes, revealing that Myc induction of amino acid transport is pivotal for subsequent bioenergetic and biosynthetic programs and licences T cell receptor driven proteome reprogramming.

immunology↗