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Biology subjects

Lozano, T.

Publications and source records attributed to Lozano, T..

3 recordsLinked to original sources

Rapid and dynamic reprogramming within the tumor microenvironment drives EDA-CAR-T dysfunction and compromised therapeutic efficacy in solid tumors

BackgroundChimeric antigen receptor (CAR)-T cell therapies efficacy in solid tumors remains limited, largely due to the profoundly immunosuppressive tumor microenvironment (TME) which drives CAR-T cells to dysfunction and poor persistence. A comprehensive understanding of the dynamic interplay between CAR-T cells and the TME is therefore critical for the rational design of more effective CAR-T strategies for solid cancers. MethodsHere, we performed single-cell RNA sequencing of tumor samples from immunocompetent mice treated with stroma-targeting EDA-CAR-T cells, profiling CAR-T cell states and TME programs at the peak of antitumor response and during subsequent tumor progression. ResultsOur analysis revealed a marked temporal remodeling of EDA-CAR-T cells within the TME, where early antitumor efficacy is associated with concurrent expansion of cytotoxic effector CD8 CAR-T cells and activation of memory CD4 CAR-T subsets. Moreover, EDA-CAR-T cells effectively engaged the myeloid compartment, resulting in strengthened communication networks involving T cell activation. However, by tumor progression, EDA-CAR-T cells suffered a widespread transcriptional reprogramming towards dysfunction, characterized by loss of effector programs alongside induction of exhaustion and immunoregulatory pathways within the TME, including PD-L1/PD-L2 and TGF{beta} signaling, which impairs sustained immune responses. Notably, early CAR-T cell activation led to increased susceptibility to TME-mediated immunosuppression, revealing EDA-CAR-T-specific soluble galectin-mediated cell-to-cell interaction networks. ConclusionsTogether, this works offers a high-resolution view of CAR-T cell dynamics within the solid TME, uncovering cellular and molecular mechanisms of rapid functional decline and identifying regulatory pathways within the TME that can be exploited to improve CAR-T cell therapy efficacy in solid tumors. KEY MESSAGES OF THE ARTICLEO_ST_ABSWhat is already known on this topicC_ST_ABSThe determinants of CAR-T cell therapeutic efficacy in solid tumors remain poorly defined, largely due to the complexity of the immunosuppressive tumor microenvironment. In this effort, it is necessary to perform comprehensive and detailed mechanistic studies that capture CAR-T cell dynamics within the solid tumor microenvironment to understand treatment failure. What this study addsWe performed single-cell profiling of stroma-targeting EDA-CAR-T cells, revealing their dynamic reprogramming toward dysfunction within the solid tumor microenvironment. We dissected CAR-T cell states and their cell-to-cell interactions with the tumor microenvironment across response and tumor progression and identified mechanisms linking CAR-T cell functionality and therapeutic failure. How this study might affect research, practice or policyThis study provides comprehensive mechanistic insights from an immunocompetent model that can be leveraged to identify shared determinants of CAR-T cell functionality in solid tumors and potentially guide the rational development of improved CAR-T cell therapies.

genomics↗

Single-Cell Multiomics Reveals Regulatory Mechanisms of CAR T Cell Persistence and Dysfunction in Multiple Myeloma

Understanding the mechanisms that drive chimeric antigen receptor (CAR) T cell function and persistence in multiple myeloma (MM) remains a critical challenge for improving therapeutic outcomes. In this study, we applied single-cell multiomics and gene regulatory network (GRN) analysis to characterize the transcriptional dynamics and clonal evolution of BCMA-targeted CAR T cells in longitudinally collected bone marrow (BM) and peripheral blood (PB) samples from MM patients. Our results revealed that CAR T cells infiltrating BM exhibited a more activated and exhausted phenotype compared to their PB counterparts, with key transcriptional regulators driving these changes. Dysregulation in the effector-to-memory transition led to an increased presence of terminally differentiated CAR T cells, correlating with poor persistence. Additionally, we identified a hyperexpanded CAR T clone in the BM of a patient with partial response, marked by elevated IL10 expression. Functional analyses demonstrated that stimulation of endogenous TCR enhanced IL10 production, potentially contributing to impaired CAR T cell proliferation and persistence. These findings uncover critical regulatory mechanisms influencing CAR T cell dynamics, offering new insights into improving CAR T cell persistence and therapeutic efficacy in MM and highlights potential molecular targets for optimizing CAR T cell therapy in patients with MM.

genomics↗

The transcriptional regulator Sin3A balances IL-17A and Foxp3 expression in primary CD4 T cells

The Sin3 transcriptional regulator homolog A (Sin3A) is the core member of a multi-protein chromatin-modifying complex known to control gene transcription via epigenetic mechanisms. Its inactivation in developing thymocytes halts T cell maturation. We and others had previously shown that Sin3A controls STAT3 transcriptional activity. Given the role of STAT3 in the differentiation of T helper 17 cells critical in inflammatory disorders and against opportunistic infections, we asked whether Sin3A could also contribute to their differentiation. To this aim, we exploited CD4-Cre and CD4-CreERT2deleter strains for conditional and inducible Sin3A deletion in CD4 cell subsets. We report that Sin3A inactivation in vivo arrested thymocyte development at the double positive stage, hindering the characterization of mature T cells. At difference, tamoxifen-inducible Sin3A deletion proved permissive for in vitro proliferation of T cells in Th17 skewing conditions and the acquisition of memory markers. Transcriptional profiling indicated that while Sin3A inactivation imprinted T cells with a mTORC1 signaling gene signature, Sin3A deficient cells lacked the expression of IL-17A, the signature Th17 cytokine. This reflected a defective induction of Il17a, and also of the Il23R and Il22 genes, which occurred in spite of proper upregulation of the lineage defining transcription factor ROR{gamma}t. We found that Sin3A inactivation was paralleled by increased STAT3 phosphorylation and nuclear representation, and by higher fractions of IL-2 and FoxP3 expressing cells. Such events proved causally linked as inhibiting Foxp3 partially rescued IL-17A expression, and neutralizing IL-2 simultaneously lowered the representation of FoxP3+cells, while rescuing IL- 17A+ ones. Thus, together our data underline a previously unappreciated role for Sin3A in Th17 differentiation and the shaping of their immunoregulatory potential. StatementThis study identifies a new role for the transcriptional regulator Sin3A in the shaping of Th17 cell differentiation. Data indicate that by controlling IL-2 expression, and mTORC1 signaling, it balances IL-17A and Foxp3 levels, shaping Th17 inflammatory potentials.

immunology↗