Silvia Lonardi

ORCID: 0000-0003-0307-4163
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About
Contact & Profiles
Research Areas
  • Immunotherapy and Immune Responses
  • Immune Cell Function and Interaction
  • Immune cells in cancer
  • Lymphoma Diagnosis and Treatment
  • Histiocytic Disorders and Treatments
  • T-cell and B-cell Immunology
  • Monoclonal and Polyclonal Antibodies Research
  • Melanoma and MAPK Pathways
  • CAR-T cell therapy research
  • Immune Response and Inflammation
  • RNA Interference and Gene Delivery
  • Fibroblast Growth Factor Research
  • Cutaneous lymphoproliferative disorders research
  • Viral-associated cancers and disorders
  • Sarcoma Diagnosis and Treatment
  • Cancer Immunotherapy and Biomarkers
  • Cancer Research and Treatments
  • Cancer Cells and Metastasis
  • Cancer, Lipids, and Metabolism
  • Cell Adhesion Molecules Research
  • Phagocytosis and Immune Regulation
  • Tumors and Oncological Cases
  • Histone Deacetylase Inhibitors Research
  • Chemokine receptors and signaling
  • Cholangiocarcinoma and Gallbladder Cancer Studies

University of Brescia
2016-2025

Istituto Oncologico Veneto
2023-2024

Istituti di Ricovero e Cura a Carattere Scientifico
2023-2024

Azienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia
2012-2024

Brescia University
2014-2024

Center for Translational Molecular Medicine
2021

MGH Institute of Health Professions
2014

Vanderbilt University
2014

Seattle University
2014

Henry Ford Hospital
2014

Abstract Technological advances have greatly improved our knowledge of myelopoiesis, for example, with the discovery granulocyte‒monocyte‒dendritic cell (DC) progenitors (GMDPs), monocyte‒DC (MDPs), common DC (CDPs) and monocyte (cMoPs) on basis flow cytometry approaches. Concomitantly, some progress has been made in characterizing very early phases human neutropoiesis description novel CD66b + progenitors, including eNePs, PMs w/o ProNeus, PreNeus. More recently, we identified four SSC lo...

10.1038/s41423-025-01259-w article EN cc-by Cellular and Molecular Immunology 2025-02-13

To date, no good marker for screening or disease monitoring of endometrial cancer (EC) is available. The aims this study were to investigate HE4 gene, protein expression and serum (sHE4) levels in a panel ECs normal endometria (NEs) correlate sHE4 with patient clinicopathological characteristics prognosis.Using quantitative real-time PCR we tested 46 20 NEs gene expression. Protein was analysed by immunohistochemistry on tissue microarrays 153 33 NEs. Pre-operative samples from 138 EC 76 NE...

10.1038/bjc.2011.109 article EN cc-by-nc-sa British Journal of Cancer 2011-04-01

<h3>Objective:</h3> To determine whether the activation of innate immune responses, which can be elicited by pathogenic and endogenous triggers, is associated with presence Epstein-Barr virus (EBV) infection in multiple sclerosis (MS) brain. <h3>Methods:</h3> White matter postmortem MS (n = 10) control tissue 11) was analyzed for expression proinflammatory cytokine interferon α (IFNα) immunohistochemistry EBV using highly sensitive method EBV-encoded RNA (EBER) situ hybridization....

10.1212/wnl.0b013e31823ed057 article EN Neurology 2011-12-08

Bone marrow (BM) metastasis remains one of the main causes death associated with solid tumors as well multiple myeloma (MM). Targeting BM niche to prevent or modulate has not been successful date. Here, we show that stromal cell-derived factor-1 (SDF-1/CXCL12) is highly expressed in active MM, sites tumor and report on discovery high-affinity anti-SDF-1 PEGylated mirror-image l-oligonucleotide (olaptesed-pegol). In vivo confocal imaging showed SDF-1 levels are increased within MM...

10.1016/j.celrep.2014.08.042 article EN cc-by-nc-nd Cell Reports 2014-09-25

Significance Macrophages can be functionally reprogrammed by the tumor microenvironment to further growth and malignancy. In this study, we have discovered that pathological process is dependent on ERK5 MAPK. Accordingly, demonstrated inactivation of in macrophages blocked phosphorylation STAT3, a transcription factor crucial for determining macrophage polarity, impaired melanoma carcinoma grafts. These results raise possibility targeting protumor via anti-ERK5 therapy constitutes very...

10.1073/pnas.1707929115 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2018-03-05

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare haematological malignancy characterized by the clonal proliferation of immature or precursors cells (PDC), also known as professional type I interferon producing cells.1 This was originally recognized in 19942 and uncertainty regarding its histogenesis reflected several changes name, that included agranular CD4+ natural killer leukemia,3 blastic leukemia/lymphoma,4 CD4+CD56+ hematodermic neoplasm5 tumor.6 In 2001 World Health...

10.4081/hmr.v3i3.553 article EN Hematology Meeting Reports (formerly Haematologica Reports) 2009-06-12

During the past few years, a number of studies reported that different melanoma cell lines could be extensively lysed in vitro by IL ‐2‐activated NK cells at appropriate effector/target ratios. Here, we show, histological evaluation lesions, /target‐cell ratios compatible with those allowing efficient killing are hardly reached tumor site. We then investigated outcome cocultures established low /melanoma After initial ‐mediated lysis, residual acquired resistance to cells. This reflected...

10.1002/eji.201142179 article EN European Journal of Immunology 2012-05-14

The homeostatic chemokine CXCL13 is preferentially produced in B-follicles and crucial the lymphoid organ development by attracting B-lymphocytes that express its selective receptor CXCR5. Follicular dendritic cells (FDCs) have been identified as main cellular source of this organs. Recently, genome-wide approaches suggested follicular CD4 T-helper (T(H)F) additional producers germinal centre neoplastic counterpart T(H)F (CD4+ tumour T-cells angioimmunoblastic T-cell lymphoma) retains...

10.1002/path.2420 article EN The Journal of Pathology 2008-07-31

Viral infections have been linked to the onset of type I diabetes (T1D), with viruses postulated induce disease directly by causing β cell injury and subsequent release autoantigens indirectly via host interferon (IFN-I) response triggered virus. Consistent this, resistance T1D is associated polymorphisms that impair function melanoma differentiation gene-5 (MDA5), a sensor viral RNA elicits IFN-I responses. In animal models, triggering another sensor, TLR3, has implicated in diabetes. Here,...

10.1172/jci44005 article EN Journal of Clinical Investigation 2011-03-14
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