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L'elaborato mira ad esplorare eventuali spazi di riforma nella disciplina penalistica delle scelte di fine vita, alla luce delle recenti evoluzioni legislative e giurisprudenziali, italiane e non solo. La ricerca si è focalizzata, in primis, sull’evoluzione della disciplina italiana in tema di omicidio del consenziente ed aiuto al suicidio. Attraverso un’indagine storica, che ha preso le mosse dalla dottrina e dalla legislazione del XVIII secolo e si è snodata soprattutto attraverso i lavori preparatori dei codici Zanardelli e Rocco, si sono evidenziate le ragioni di fondo della politica criminale sul punto ed i punti critici su cui si è soffermata la dottrina. L’analisi delle fattispecie penali vigenti è stata accompagnata dall’esame della giurisprudenza dell’ultimo ventennio, che ha fortemente contribuito ad “attualizzare” la tutela offerta ai c.d. “soggetti deboli” e a risolvere i conflitti tra beni giuridici in gioco, prendendo atto dell’evoluzione delle conoscenze scientifiche e dell’emersione di scenari inimmaginabili per il legislatore del 1930. Ciò nonostante, la ricerca ha evidenziato che, anche dopo la rivoluzionaria sentenza n. 242 del 2019 della Corte costituzionale sull’art. 580 c.p., permangono forti profili di criticità dovuti all’applicazione di norme risalenti, ritenute inadeguate rispetto al contesto sociale odierno, e a formulazioni testuali foriere di dubbi interpretativi. All’esito di queste valutazioni, sono stati identificati alcuni aspetti cruciali per una possibile riforma legislativa e si è ritenuto opportuno esplorare anche le scelte effettuate da altri ordinamenti europei, al fine di identificare buone pratiche da cui trarre spunto. Alla luce delle conoscenze acquisite grazie all’analisi comparata, l’elaborato avanza, infine, alcune proposte di riforma, anche facendo riferimento alle proposte di legge già depositate in Parlamento, e dà atto della pendenza di una proposta di referendum parzialmente abrogativo dell’art. 579 c.p. (s, The paper aims to explore possible spaces to reform the criminal discipline of end-of-life choices, expecially after the recent legislative and jurisprudential developments, both in Italy and beyond. The research focused, first of all, on the evolution of the Italian discipline in terms of murder with the consent of the victim and contribution to others’ suicide. Through a historical investigation, which begin with an investigation about the legal doctrine and the legislation of the 18th century and developed above all through the preparatory work of the Zanardelli and Rocco codes, the underlying reasons for the criminal policy on this point and the critical points on which the doctrine has focused are highlighted. The analysis of the criminal offenses in force is accompanied by an examination of the jurisprudence of the last twenty years, which has greatly contributed to "updating" the protection offered to the so-called "weak subjects" and to resolve the conflicts between legal assets at stake, taking note of the evolution of scientific knowledge and the emergence of unimaginable scenarios for the legislator of 1930. Nevertheless, research has shown that, even after the revolutionary ruling n. 242/2019 of the Constitutional court about art. 580 of the criminal code, there are still strong critical issues due to the application of outdated rules, deemed inadequate if compared with today's social context, and to textual formulations which may contribute to the emergence of interpretative difficulties. As a result of these assessments, some crucial aspects were identified for a possible legislative reform and it was considered appropriate to also explore the choices made by other European systems, in order to identify good practices from which to draw inspiration. In light of the knowledge acquired thanks to the comparative analysis, the paper finally puts forward some reform proposals, also referring to the bills already filed in Parliament, and acknowledges the pen more...

Background: Severe early-onset erythroderma and gut inflammation, with massive tissue infiltration of oligoclonal activated T cells are the hallmark of Omenn syndrome (OS). Objective: The impact of altered gut homeostasis in the cutaneous manifestations of OS remains to be clarified. Methods: We analyzed a cohort of 15 patients with OS and the 129Sv/C57BL/6 knock-in Rag2R229Q/R229Q (Rag2R229Q) mouse model. Homing phenotypes of circulating lymphocytes were analyzed by flow cytometry. Inflammatory cytokines and chemokines were examined in the sera by ELISA and in skin biopsies by immunohistochemistry and in situ RNA hybridization. Experimental colitis was induced in mice by dextran sulfate sodium salt. Results: We show that memory/activated T cells from patients with OS and from the Rag2R229Q mouse model of OS abundantly express the skin homing receptors cutaneous lymphocyte associated antigen and CCR4 (Ccr4), associated with high levels of chemokine C-C motif ligands 17 and 22. Serum levels of LPS are also elevated. A broad TH1/TH2/TH17 inflammatory signature is detected in the periphery and in the skin. Increased Tlr4 expression in the skin of Rag2R229Q mice is associated with enhanced cutaneous inflammation on local and systemic administration of LPS. Likewise, boosting colitis in Rag2R229Q mice results in increased frequency of Ccr4+ splenic T cells and worsening of skin inflammation, as indicated by epidermal thickening, enhanced epithelial cell activation, and dermal infiltration by TH1 effector T cells. Conclusions: These results support the existence of an interplay between gut and skin that can sustain skin inflammation in OS. more...

Omenn syndrome (OS) is caused by hypomorphic Rag mutations and characterized by a profound immunodeficiency associated with autoimmune-like manifestations. Both in humans and mice, OS is mediated by oligoclonal activated T and B cells. The role of microbial signals in disease pathogenesis is debated. Here, we show that Rag2R229Q knock-in mice developed an inflammatory bowel disease affecting both the small bowel and colon. Lymphocytes were sufficient for disease induction, as intestinal CD4 T cells with a Th1/Th17 phenotype reproduced the pathological picture when transplanted into immunocompromised hosts. Moreover, oral tolerance was impaired in Rag2R229Q mice, and transfer of wild-type (WT) regulatory T cells ameliorated bowel inflammation. Mucosal immunoglobulin A (IgA) deficiency in the gut resulted in enhanced absorption of microbial products and altered composition of commensal communities. The Rag2R229Q microbiota further contributed to the immunopathology because its transplant into WT recipients promoted Th1/Th17 immune response. Consistently, long-term dosing of broad-spectrum antibiotics (ABXs) in Rag2R229Q mice ameliorated intestinal and systemic autoimmunity by diminishing the frequency of mucosal and circulating gut-tropic CCR9+ Th1 and Th17 T cells. Remarkably, serum hyper-IgE, a hallmark of the disease, was also normalized by ABX treatment. These results indicate that intestinal microbes may play a critical role in the distinctive immune dysregulation of OS. more...

Pentraxin 3 (PTX3) is a fluid-phase pattern recognition molecule and a key component of the humoral arm of innate immunity. In four different models of tissue damage in mice, PTX3 deficiency was associated with increased fibrin deposition and persistence, and thicker clots, followed by increased collagen deposition, when compared with controls. Ptx3-deficient macrophages showed defective pericellular fibrinolysis in vitro. PTX3-bound fibrinogen/fibrin and plasminogen at acidic pH and increased plasmin-mediated fibrinolysis. The second exon-encoded N-terminal domain of PTX3 recapitulated the activity of the intact molecule. Thus, a prototypic component of humoral innate immunity, PTX3, plays a nonredundant role in the orchestration of tissue repair and remodeling. Tissue acidification resulting from metabolic adaptation during tissue repair sets PTX3 in a tissue remodeling and repair mode, suggesting that matrix and microbial recognition are common, ancestral features of the humoral arm of innate immunity. more...

Pentraxin 3 (PTX3) is a fluid-phase pattern recognition molecule and a key component of the humoral arm of innate immunity. In four different models of tissue damage in mice, PTX3 deficiency was associated with increased fibrin deposition and persistence, and thicker clots, followed by increased collagen deposition, when compared with controls. Ptx3-deficient macrophages showed defective pericellular fibrinolysis in vitro. PTX3-bound fibrinogen/fibrin and plasminogen at acidic pH and increased plasmin-mediated fibrinolysis. The second exon-encoded N-terminal domain of PTX3 recapitulated the activity of the intact molecule. Thus, a prototypic component of humoral innate immunity, PTX3, plays a nonredundant role in the orchestration of tissue repair and remodeling. Tissue acidification resulting from metabolic adaptation during tissue repair sets PTX3 in a tissue remodeling and repair mode, suggesting that matrix and microbial recognition are common, ancestral features of the humoral arm of innate immunity. more...