0000000000217485

AUTHOR

Luigi Ruco

showing 6 related works from this author

Follicular dendritic cells display microvesicle-associated LMP1 in reactive germinal centers of EBV+ classic Hodgkin lymphoma

2018

Expression of the latent membrane protein-1 (LMP1) of Epstein-Barr virus (EBV) was investigated in 153 cases of EBV+ classic Hodgkin lymphoma (cHL); 120 cases were pediatric patients (< 14 years of age) from Iraq, and 33 cases were adult patients from Italy. We describe for the first time the presence of LMP1 protein in EBV-encoded RNA (EBER)-negative follicular dendritic cells (FDCs) of reactive germinal centers (GC) associated with EBV+ cHL. Presence of LMP1+ GCs was independent of geographic region and age of patients. Variable numbers of reactive GCs were present in 22.2% of cases (34 of 153), whereas LMP1 staining of FDCs was present in about a third of cases (10 of 34) with reactiv…

0301 basic medicineMaleEpstein-Barr Virus InfectionsClassic Hodgkin lymphoma (cHL)CD30Follicular dendritic cells (FDCs)Exosomes and&nbsp0302 clinical medicineclassic hodgkin lymphoma (chl); epstein-barr virus (ebv); exosomes and microvesicles; follicular dendritic cells (fdcs); latent membrane protein-1 (lmp1); programmed death ligand 1 (pd-l1)Nodular sclerosisCell-Derived MicroparticlesEpstein-Barr Virus Infectionhemic and lymphatic diseasesChildCD63MicrovesicleGeneral MedicineMiddle AgedHodgkin DiseaseEpstein-Barr virus (EBV)Cell-Derived Microparticle030220 oncology & carcinogenesisProgrammed death ligand 1 (PD-L1)microvesicleOriginal ArticleFemaleHumanAdultBiologyVirusPathology and Forensic MedicineViral Matrix Proteins03 medical and health sciencesExosomes and microvesiclesmedicineotorhinolaryngologic diseasesHumansMolecular BiologyEpstein–Barr virus infectionAgedFollicular dendritic cellsGerminal centerCell Biologymedicine.diseaseGerminal CenterMolecular biologystomatognathic diseases030104 developmental biologyLatent membrane protein-1 (LMP1)Dendritic Cells Follicular
researchProduct

A practical algorithmic approach to mature aggressive B cell lymphoma diagnosis in the double/triple hit era. Selecting cases, matching clinical bene…

2019

An accurate diagnosis of clinically distinct subgroups of aggressive mature B cell lymphomas is crucial for the choice of proper treatment. Presently, precise recognition of these disorders relies on the combination of morphological, immunophenotypical, and cytogenetic/molecular features. The diagnostic workup in such situations implies the application of costly and time-consuming analyses, which are not always required, since an intensified treatment option is reasonably reserved to fit patients. The Italian Group of Haematopathology proposes herein a practical algorithm for the diagnosis of aggressive mature B cell lymphomas based on a stepwise approach, aimed to select cases deserving mo…

0301 basic medicinemedicine.medical_specialtyMatching (statistics)Lymphoma B-CellLymphomadouble hitComputer scienceMYCDouble hitFluorescencePathology and Forensic MedicineImmunophenotyping03 medical and health sciences0302 clinical medicineFISHDiagnosismedicinePractical algorithmHumansIntensive care medicineB-cell lymphomaMolecular BiologyIn Situ HybridizationIn Situ Hybridization FluorescenceHGBLBrief ReportB-CellTreatment optionsCorrectionDiagnosis; DLBCL; Double hit; FISH; HGBL; MYC; Humans; Immunophenotyping; In Situ Hybridization Fluorescence; Lymphoma B-Cell; AlgorithmsCell BiologyGeneral MedicineDiagnosis DLBCL Double hit FISH HGBL MYCmedicine.diseaseDiagnosis; DLBCL; double hit; FISH; HGBL; MYCOptimal managementMolecular analysis030104 developmental biology030220 oncology & carcinogenesisDLBCLPosition paperProper treatmentAlgorithmsDiagnosiHuman
researchProduct

Rituximab plus chemotherapy provides no clinical benefit in a peripheral T-cell lymphoma not otherwise specified with aberrant expression of CD20 and…

2020

Peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) is the most common entity of mature T-cell neoplasms. PTCL-NOS generally has an aggressive behavior and is often refractory to standard therapy. Only a few cases of PTCL with aberrant expression of B-cell antigens have been reported so far. This phenotypic aberrancy may lead to misdiagnosis as B-cell non-Hodgkin lymphomas and eventual inappropriate patient management, whereas in an accurately diagnosed PTCL, the presence of CD20 may appear as an appealing therapeutic target. In this setting, response to anti-CD20 monoclonal antibody in combination with chemotherapy has been poorly explored. We describe the case of a 59-year-old …

Oncologyperipheral t-cell lymphomamedicine.medical_specialtymedicine.medical_treatmentClinical BiochemistryPeripheral T-cell lymphoma not otherwise specifiedCase ReportSettore MED/08 - Anatomia Patologicarituximab.03 medical and health sciences0302 clinical medicinerituximabimmune system diseasesInternal medicinehemic and lymphatic diseasesMedicineb-cell antigens; cd20; cd79a; peripheral t-cell lymphoma; rituximabCD20cd79aperipheral T-cell lymphomaB-cell antigenCD20lcsh:R5-920Chemotherapybiologybusiness.industryNot Otherwise Specifiedcd20CD79amedicine.diseaseCD79APeripheral T-cell lymphomaLymphomab-cell antigens030220 oncology & carcinogenesisbiology.proteinRituximablcsh:Medicine (General)business030215 immunologymedicine.drug
researchProduct

Control of target cell survival in thyroid autoimmunity by T helper cytokines via regulation of apoptotic proteins

2000

After autoimmune inflammation, interactions between CD95 and its ligand (CD95L) mediate thyrocyte destruction in Hashimoto's thyroiditis (HT). Conversely, thyroid autoimmune processes that lead to Graves' disease (GD) result in autoantibody-mediated thyrotropin receptor stimulation without thyrocyte depletion. We found that GD thyrocytes expressed CD95 and CD95L in a similar manner to HT thyrocytes, but did not undergo CD95-induced apoptosis either in vivo or in vitro. This pattern was due to the differential production of TH1 and TH2 cytokines. Interferon gamma promoted caspase up-regulation and CD95-induced apoptosis in HT thyrocytes, whereas interleukin 4 and interleukin 10 protected GD …

Adultendocrine systemmedicine.medical_specialtyFas Ligand Proteinendocrine system diseasesCell SurvivalImmunologyCASP8 and FADD-Like Apoptosis Regulating ProteinThyroid Glandbcl-X ProteinApoptosisMice TransgenicIn Vitro TechniquesThyroiditisThyrotropin receptorMiceTh2 CellsSettore MED/04 - PATOLOGIA GENERALEInternal medicinemedicineImmunology and AllergyAnimalsHumansInterferon gammafas ReceptorInterleukin 4CaspaseMembrane GlycoproteinsbiologyThyroidIntracellular Signaling Peptides and ProteinsThyroiditis AutoimmuneT-Lymphocytes Helper-InducerMiddle AgedTh1 CellsFas receptormedicine.diseaseGraves DiseaseInterleukin 10medicine.anatomical_structureEndocrinologyProto-Oncogene Proteins c-bcl-2biology.proteinCytokinesCarrier Proteinsmedicine.drug
researchProduct

Response to 'TH1 and TH2 cytokine control of thyrocyte survival in thyroid autoimmunity'

2001

Mirakian et al. question our recent results, which suggest that thyrocyte survival during thyroid autoimmunity depends on differential effects of TH1 and TH2 cytokines1. Thyrocyte destruction in autoimmune thyroiditis is a slow process that lasts several years. We hypothesized that in thyroid autoimmunity the balance between life and death in thyrocytes depends on the predominance over the time of TH2 and TH1 cytokines, whose action is not restricted to immune cells but involves direct modulation of key molecules responsible for survival or death of target cells1.

business.industrymedicine.medical_treatmentImmunologymedicine.diseaseDifferential effectsAutoimmune thyroiditisCytokineImmune systemImmunologyThyroid autoimmunitymedicineImmunology and AllergyTh1 cytokinesbusinessNature Immunology
researchProduct

Transglutaminase Type II Plays a Protective Role in Hepatic Injury

2003

The up-regulation of "tissue" transglutaminase (TG2) gene has been shown to occur in various pathologies and can lead to severe liver injury; however, its role in the onset of liver damage has not yet been clarified. To address this issue, we have used two experimental settings: carbon tetrachloride (CCl(4))-induced liver injury in wild-type and TG2 knockout mice; and liver biopsies obtained from a large cohort of hepatitis C virus (HCV)-infected patients. Mice lacking TG2 failed to clear the hepatic necrotic tissue formed in response to prolonged CCl(4) exposure (5 weeks) and 60% of them died before the end of the treatment. By contrast, wild-type mice were able to recover after the toxic …

AdultPathologymedicine.medical_specialtyNecrosisGenotypeTissue transglutaminaseHepatitis C virusCCL4medicine.disease_causeGene Expression Regulation EnzymologicPathology and Forensic MedicineExtracellular matrixMiceNecrosisGTP-Binding ProteinsmedicineAnimalsHumansProtein Glutamine gamma Glutamyltransferase 2Mice KnockoutHepatitisLiver injuryTransglutaminasesbiologyCarbon Tetrachloride PoisoningHepatitis C ChronicMiddle Agedmedicine.diseaseMice Inbred C57BLLiverKnockout mousebiology.proteinmedicine.symptomRegular ArticlesThe American Journal of Pathology
researchProduct