Author
Mauro Di Ianni
Other affiliations: University of Perugia
Bio: Mauro Di Ianni is an academic researcher from University of L'Aquila. The author has contributed to research in topics: Transplantation & Hematopoietic stem cell transplantation. The author has an hindex of 22, co-authored 61 publications receiving 3242 citations. Previous affiliations of Mauro Di Ianni include University of Perugia.
Papers published on a yearly basis
Papers
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TL;DR: It is shown for the first time in humans that adoptive transfer of Tregs prevented GVHD in the absence of any posttransplantation immunosuppression, promoted lymphoid reconstitution, improved immunity to opportunistic pathogens, and did not weaken the graft-versus-leukemia effect.
982 citations
TL;DR: It is demonstrated the immunosuppressive potential of Tregs can be used to suppress GVHD without loss of the benefits of graft-versus-leukemia (GVL) activity, and humanized murine models provided insights into the mechanisms underlying separation of GVL from GV HD.
332 citations
TL;DR: It is demonstrated that MSCs recruit, regulate, and maintain T-regulatory phenotype and function over time.
312 citations
TL;DR: The findings show that Notch signaling plays a critical role in B-CLL cell survival and apoptosis resistance and suggest that it could be a novel potential therapeutic target.
294 citations
TL;DR: It is found that the presence of the DECTIN1 Y238X polymorphism in either donors or recipients of hematopoietic stem cell transplantation increased susceptibility to aspergillosis, with the risk being highest when the polymorphism was present simultaneously in both donors and recipients.
260 citations
Cited by
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University of Texas Health Science Center at San Antonio1, University of California, Davis2, University Hospital of South Manchester NHS Foundation Trust3, Harvard University4, Tufts University5, University of Strasbourg6, University of Texas MD Anderson Cancer Center7, Johns Hopkins University8, University of Minnesota9, University of Pittsburgh10, Roswell Park Cancer Institute11, Duke University12, Cornell University13, University of Florida14, National Institutes of Health15
TL;DR: IDSA considers adherence to these guidelines to be voluntary, with the ultimate determination regarding their application to be made by the physician in the light of each patient's individual circumstances.
Abstract: It is important to realize that guidelines cannot always account for individual variation among patients. They are not intended to supplant physician judgment with respect to particular patients or special clinical situations. IDSA considers adherence to these guidelines to be voluntary, with the ultimate determination regarding their application to be made by the physician in the light of each patient's individual circumstances.
1,745 citations
TL;DR: Research in this field is entering an exciting period of transition from studying the molecular and cellular bases of fungal virulence to determining the cellular and molecular mechanisms that maintain immune homeostasis with fungi.
Abstract: Fungal diseases represent an important paradigm in immunology, as they can result from either a lack of recognition by the immune system or overactivation of the inflammatory response. Research in this field is entering an exciting period of transition from studying the molecular and cellular bases of fungal virulence to determining the cellular and molecular mechanisms that maintain immune homeostasis with fungi. The fine line between these two research areas is central to our understanding of tissue homeostasis and its possible breakdown in fungal infections and diseases. Recent insights into immune responses to fungi suggest that functionally distinct mechanisms have evolved to achieve optimal host-fungus interactions in mammals.
1,528 citations
TL;DR: The patterns of somatic mutation, supported by functional and clinical analyses, strongly indicate that the recurrent NOTCH1, MYD88 and XPO1 mutations are oncogenic changes that contribute to the clinical evolution of the disease.
Abstract: Chronic lymphocytic leukaemia (CLL), the most frequent leukaemia in adults in Western countries, is a heterogeneous disease with variable clinical presentation and evolution. Two major molecular subtypes can be distinguished, characterized respectively by a high or low number of somatic hypermutations in the variable region of immunoglobulin genes. The molecular changes leading to the pathogenesis of the disease are still poorly understood. Here we performed whole-genome sequencing of four cases of CLL and identified 46 somatic mutations that potentially affect gene function. Further analysis of these mutations in 363 patients with CLL identified four genes that are recurrently mutated: notch 1 (NOTCH1), exportin 1 (XPO1), myeloid differentiation primary response gene 88 (MYD88) and kelch-like 6 (KLHL6). Mutations in MYD88 and KLHL6 are predominant in cases of CLL with mutated immunoglobulin genes, whereas NOTCH1 and XPO1 mutations are mainly detected in patients with unmutated immunoglobulins. The patterns of somatic mutation, supported by functional and clinical analyses, strongly indicate that the recurrent NOTCH1, MYD88 and XPO1 mutations are oncogenic changes that contribute to the clinical evolution of the disease. To our knowledge, this is the first comprehensive analysis of CLL combining whole-genome sequencing with clinical characteristics and clinical outcomes. It highlights the usefulness of this approach for the identification of clinically relevant mutations in cancer.
1,435 citations
TL;DR: Some of the molecules involved in the paracrine effects of MSCs are identified with a perspective that these cells intrinsically belong to a perivascular niche in vivo, and how this knowledge could be advantageously used in clinical applications is discussed.
1,254 citations