Clorinda Fusco

University of Naples Federico II

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Co-Authors

Giuseppe Matarese

University of Naples Federico II

Alessandra Colamatteo

University of Naples Federico II

Veronica De Rosa

Institute for Experimental Endocrinology and Oncology

Paola de Candia

University of Naples Federico II

Sara Bruzzaniti

Institute for Experimental Endocrinology and Oncology

Mario Galgani

Institute for Experimental Endocrinology and Oncology

Teresa Micillo

University of Naples Federico II

Claudio Procaccini

Institute for Experimental Endocrinology and Oncology

Francesca Di Rella

Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale"

Antonio Porcellini

Istituto Nazionale di Fisica Nucleare, Sezione di Napoli

Cooperative Institutions

University of Naples Federico II

Istituti di Ricovero e Cura a Carattere Scientifico

Federico II University Hospital

National Research Council

Institute for Experimental Endocrinology and Oncology

Istituto Neurologico Mediterraneo

Fondazione Santa Lucia

University of Salerno

University of Campania "Luigi Vanvitelli"

University of Rome Tor Vergata

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Caloric Restriction Promotes Immunometabolic Reprogramming Leading to Protection from Tuberculosis

Cell Metabolism (2021)

Carla Palma Claudia La Rocca Vincenzo Gigantino Gabriella Aquino Giovanni Piccaro

Reprogramming

Pathogenesis

10.1016/j.cmet.2020.12.016

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Citations (51)

Metabolomics, Lipidomics, and Immunometabolism

Methods in molecular biology (2021)

Fortunata Carbone Sara Bruzzaniti Clorinda Fusco Alessandra Colamatteo Teresa Micillo

Lipidome

Metabolome

Metabolic pathway

10.1007/978-1-0716-1311-5_24

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Citations (9)

Metabolism and Autoimmune Responses: The microRNA Connection

Frontiers in Immunology (2019)

Alessandra Colamatteo Teresa Micillo Sara Bruzzaniti Clorinda Fusco S. Garavelli

Distinct metabolic pathways are known to regulate growth, differentiation, survival and activation of immune cells by providing energy and specific biosynthetic precursors. Compelling experimental evidence demonstrates that effector T cell functions are coupled with profound changes in cellular metabolism. Importantly, the effector T cell-dependent "anti-self" response characterizing the autoimmune diseases is accompanied by significant metabolic alterations. MicroRNAs (miRNAs), evolutionary conserved small non-coding RNA molecules that affect gene expression by binding to target messenger RNAs, are now known to regulate multiple functions of effector T cells, including the strength of their activation, thus contributing to immune homeostasis. In this review, we will examine the most recent studies that describe miRNA direct involvement in the metabolic reprogramming that marks effector T cell functions. In particular, we will focus on the work showing a connection between miRNA regulatory function and the molecular network dysregulation that leads to metabolic pathway derangement in autoimmunity. Finally, we will also speculate on the possibility that the interplay between miRNAs and metabolism in T cells may help identifying novel miRNA-based therapeutic strategies to treat effector T cell immunometabolic alterations in pathological conditions such as autoimmunity and chronic inflammation.

Reprogramming

10.3389/fimmu.2019.01969

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Citations (32)

Type 2 Diabetes: How Much of an Autoimmune Disease?

Frontiers in Endocrinology (2019)

Paola de Candia Francesco Prattichizzo S. Garavelli Veronica De Rosa Mario Galgani

Type 2 diabetes (T2D) is characterized by a progressive status of chronic, low-grade inflammation (LGI) that accompanies the whole trajectory of the disease, from its inception to complication development. Accumulating evidence is disclosing a long list of possible "triggers" of inflammatory responses, many of which are promoted by unhealthy lifestyle choices and advanced age. Diabetic patients show an altered number and function of immune cells, of both innate and acquired immunity. Reactive autoantibodies against islet antigens can be detected in a subpopulation of patients, while emerging data are also suggesting an altered function of specific T lymphocyte populations, including T regulatory (Treg) cells. These observations led to the hypothesis that part of the inflammatory response mounting in T2D is attributable to an autoimmune phenomenon. Here, we review recent data supporting this framework, with a specific focus on both tissue resident and circulating Treg populations. We also propose that selective interception (or expansion) of T cell subsets could be an alternative avenue to dampen inappropriate inflammatory responses without compromising immune responses.

Prediabetes

10.3389/fendo.2019.00451

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Citations (105)

PTX3: an inflammatory protein modulating ultrastructure and bioenergetics of human endothelial cells

Immunity & Ageing (2019)

Albino Carrizzo Claudio Procaccini Paola Lenzi Clorinda Fusco Francesco Villa

Pentraxin 3 (PTX3), an acute-phase inflammation protein produced by several cell types, has long been described as a possible biomarker for age-related cardiovascular and cerebrovascular diseases. Although several mechanisms of action have been identified to date in the vascular and immune systems, the direct effects of PTX3 on isolated endothelial cells at morphological and metabolic levels remain unknown.PTX3 induced cytoplasmic vacuolization and dilution of mitochondrial matrix in isolated, human endothelial cells. Moreover, metabolic assays revealed that PTX3 increases respiratory capacity in support of mitochondrial function, and partially sustains the glycolytic pathway.PTX3 has, per se, a direct action on ultrastructural and bioenergetic parameters of isolated endothelial cells. This finding can be associated with our previous demonstration of a deleterious effect of PTX3 on the endothelial layer. More studies are needed to clearly demonstrate any direct correlation between these ultrastructural and bioenergetic changes with endothelial dysfunction, especially with regard to age-related cerebro- and cardio-vascular diseases.

PTX3

Bioenergetics

Endothelial Dysfunction

10.1186/s12979-019-0144-0

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Citations (14)

A rapid and inexpensive genotyping method using dried blood spots for mutational analysis in a mutant mouse model: an update

Molecular Biology Reports (2022)

Antonella Romano Candida Zuchegna Giuseppa Zannini Samantha Messina Clorinda Fusco

Dried blood

Spots

10.1007/s11033-022-07649-x

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Citations (2)

CD4+Foxp3E2+ regulatory T cell frequency predicts breast cancer prognosis and recurrence

bioRxiv (Cold Spring Harbor Laboratory) (2024)

Clorinda Fusco Francesca Di Rella Antonietta Liotti Alessandra Colamatteo Anne Lise Ferrara

Abstract CD4 + Foxp3 + regulatory T cells (Tregs) are key to maintain peripheral self -tolerance and suppress immune responses to tumors. Their accumulation in the tumor microenvironment (TME) correlates with poor clinical outcome in several human cancers, including breast cancer (BC). However, the properties of intratumoral Tregs remain largely unknown. Here, we found that a functionally distinct subpopulation of tumor-infiltrating Tregs, which express the Foxp3 splicing variant retaining exon 2 (Foxp3E2), is prominent in the TME and peripheral blood of hormone receptor- positive (HR + ) BC subjects with poor prognosis. Notably, a comprehensive examination of the Tumor Cell Genome Atlas (TCGA) validated Foxp3E2 as an independent prognostic marker in all other BC subtypes. We found that FOXP3E2 expression underlies BCs with highly immune suppressive landscape, defective mismatch repair and a stem-like signature thus highlighting pathways involved in tumor immune evasion. Finally, we confirmed the higher immunosuppressive capacity of BC patients-derived Foxp3E2 + Tregs by functional assays. Our study suggests Foxp3E2 + Tregs might be used as an independent biomarker to predict BC prognosis and recurrence, and to develop super-targeted depletion-based immunotherapies. One-sentence summaries Foxp3E2 + Treg enrichment reflects an increased tumor-immune suppression and predicts prognosis and recurrence in breast cancer.

10.1101/2024.09.04.611142

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Citations (0)

Cellular and molecular signaling towards T cell immunological self-tolerance

Journal of Biological Chemistry (2024)

Fortunata Carbone Claudia Russo Alessandra Colamatteo Claudia La Rocca Clorinda Fusco

CD80

Peripheral tolerance

CD86

10.1016/j.jbc.2024.107134

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Citations (1)

Molecular Mechanisms Controlling Foxp3 Expression in Health and Autoimmunity: From Epigenetic to Post-translational Regulation

Frontiers in Immunology (2020)

Alessandra Colamatteo Fortunata Carbone Sara Bruzzaniti Mario Galgani Clorinda Fusco

The discovery of the transcription factor Forkhead box-p3 (Foxp3) has shed fundamental insights into the understanding of the molecular determinants leading to generation and maintenance of T regulatory (Treg) cells, a cell population with a key immunoregulatory role. Work over the past few years has shown that fine-tuned transcriptional and epigenetic events are required to ensure stable expression of Foxp3 in Treg cells. The equilibrium between phenotypic plasticity and stability of Treg cells is controlled at the molecular level by networks of transcription factors that bind regulatory sequences, such as enhancers and promoters, to regulate Foxp3 expression. Recent reports have suggested that specific modifications of DNA and histones are required for the establishment of the chromatin structure in conventional CD4+ T (Tconv) cells for their future differentiation into the Treg cell lineage. In this review, we discuss the molecular events that control Foxp3 gene expression and address the associated alterations observed in human diseases. Also, we explore how Foxp3 inﬂuences the gene expression programs in Treg cells and how unique properties of Treg-cell subsets are deﬁned by other transcription factors.

10.3389/fimmu.2019.03136

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Citations (98)

Molecular Mechanisms Controlling Foxp3 Expression in Health and Autoimmunity: From Epigenetic to Post-translational Regulation.

Zenodo (CERN European Organization for Nuclear Research) (2020)

Alessandra Colamatteo Carbone Fortunata Sara Bruzzaniti Mario Galgani Clorinda Fusco

Translational Research

Posttranslational modification

10.5281/zenodo.3702407

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Citations (0)