0000000000891190

AUTHOR

Mario Galgani

0000-0001-8414-1676

showing 2 related works from this author

Differential impact of high and low penetrance TNFRSF1A gene mutations on conventional and regulatory CD4+ T cell functions in TNFR1-associated perio…

2015

Abstract TNFR-associated periodic syndrome is an autoinflammatory disorder caused by autosomal-dominant mutations in TNFRSF1A, the gene encoding for TNFR superfamily 1A. The lack of knowledge in the field of TNFR-associated periodic syndrome biology is clear, particularly in the context of control of immune self-tolerance. We investigated how TNF-α/TNFR superfamily 1A signaling can affect T cell biology, focusing on conventional CD4+CD25− and regulatory CD4+CD25+ T cell functions in patients with TNFR-associated periodic syndrome carrying either high or low penetrance TNFRSF1A mutations. Specifically, we observed that in high penetrance TNFR-associated periodic syndrome, at the molecular le…

Male0301 basic medicinePenetranceAutoimmunitymedicine.disease_causeT-Lymphocytes RegulatoryImmune toleranceSettore MED/38 - Pediatria Generale E SpecialisticaTRAPS; Tconvs; Tregs; autoimmunity; immune toleranceImmunology and AllergyIL-2 receptorChildGeneticsMutationTconvTOR Serine-Threonine Kinaseshemic and immune systemsMiddle AgedAcquired immune systemPenetranceTregSTAT Transcription Factorsmedicine.anatomical_structureReceptors Tumor Necrosis Factor Type ICytokinesFemalebiological phenomena cell phenomena and immunitySignal TransductionAdultAdolescentFeverT cellAutoimmunity; Immune tolerance; Tconvs; Tregs; TRAPS; Cell Biology; ImmunologyImmunologyReceptors Antigen T-CellContext (language use)Tregs[object Object]BiologyImmunophenotypingYoung Adult03 medical and health sciencesImmune systemmedicineHumansAgedCell ProliferationDemographyTconvsImmune toleranceHereditary Autoinflammatory DiseasesTRAPSCell Biologybiological factors030104 developmental biologyMutationCancer research
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Role of adipokines signaling in the modulation of T cells function

2013

The field that links immunity and metabolism is rapidly expanding. Apparently non-immunological disorders such as obesity and type 2 diabetes have been linked to immune dysregulation, suggesting that metabolic alterations can be induced by or be consequence of an altered self-immune tolerance. In this context, adipose tissue produces and releases a variety of pro-inflammatory and anti-inflammatory factors, termed "adipokines," which can be considered as the bridge between obesity-related exogenous factors, such as nutrition and lifestyle, and the molecular events leading to metabolic syndrome, inflammatory, and/or autoimmune conditions. In obesity, increased production of most adipokines im…

Leptinlcsh:Immunologic diseases. AllergyobesityImmunologyT cellsAdipose tissueAdipokineContext (language use)Review Articlemedicine.disease_cause03 medical and health sciences0302 clinical medicineImmune systemmedicineImmunology and Allergy030304 developmental biologyobesity.0303 health sciencesbusiness.industryLeptinLipid metabolismImmune dysregulationmedicine.disease3. Good health030220 oncology & carcinogenesisadipocytokinesImmunologyAdiponectinMetabolic syndromebusinesslcsh:RC581-607Frontiers in Immunology
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