About: Fabrizio Mattei

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

researcher

Attributes	Values
rdf:type	Item
description	forskare (sv) ikertzailea (eu) researcher (en) 연구원 (ko) ricercatore (it) গবেষক (bn) 研究者 (ja) ഗവേഷകൻ (ml) araştırmacı (tr) wetenschapper (nl) дослідник (uk) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy) hulumtues (sq)
rdfs:label	Fabrizio Mattei (en) Fabrizio Mattei (es) Fabrizio Mattei (nl) Fabrizio Mattei (sl) Fabrizio Mattei (ast)
skos:prefLabel	Fabrizio Mattei (en) Fabrizio Mattei (es) Fabrizio Mattei (nl) Fabrizio Mattei (sl) Fabrizio Mattei (ast)
name	Fabrizio Mattei (en) Fabrizio Mattei (es) Fabrizio Mattei (nl) Fabrizio Mattei (sl) Fabrizio Mattei (ast)
Scopus author ID	wds:Q42583827-5E850741-49C5-486B-9A6F-36ACBD5CCD69
Scopus author ID	7003675806
given name	wds:Q42583827-00B79601-161A-439B-97BA-79F4BC034118
given name	Fabrizio
instance of	wds:Q42583827-D71812A3-C6EE-499E-A784-1D21E5B45858
instance of	Homo sapiens
Loop ID	wds:Q42583827-44040FDB-D9DA-4795-A5C6-34E2AFE5503C
Loop ID	67040
skos:altLabel	Mattei Fabrizio Mattei F. (en)
occupation	wds:Q42583827-D6BB0F84-46B7-4299-8814-3174274973B1
employer	wds:Q42583827-303A7D99-EA7E-44E9-A5B0-D2A3BFD89C51
CERL Thesaurus ID	wds:Q42583827-FE724CB5-8157-45C2-B75D-13C487549182
sex or gender	wds:Q42583827-525664BA-85AF-435F-A174-24B280CE829B
VIAF ID	wds:Q42583827-2BBC1D2A-068B-465E-B4D4-A5437337A8C6
GND ID	wds:Q42583827-488679B7-6209-42B7-BF9F-2F1F45D70828
educated at	wds:Q42583827-7F31B04F-A78F-43E2-B8FC-18BE16412CD3 wds:Q42583827-D9F4ABBA-57CE-4565-9802-8605141DE49E
family name	wds:Q42583827-007F0BCA-0C13-408E-96BD-641BE5F8738C
CERL Thesaurus ID	http://thesaurus.cerl.org/record/cnp01105764
VIAF ID	http://viaf.org/viaf/40195208
GND ID	https://d-nb.info/gnd/119755513
occupation	researcher
employer	Istituto Superiore di Sanità
CERL Thesaurus ID	cnp01105764
sex or gender	male
VIAF ID	40195208
GND ID	119755513
educated at	Department of Statistical Sciences, Sapienza University of Rome
family name	Mattei
ORCID iD	wds:Q42583827-ED6BD557-BEAD-4943-B6F8-D7E39DE14F27
ORCID iD	https://orcid.org/0000-0002-5357-7773
ORCID iD	0000-0002-5357-7773
ResearcherID	wds:Q42583827-586823A3-DE73-4910-8262-F723F83337F3
Publons author ID	wds:Q42583827-fd86e769-8946-4052-adb7-0290ae84d4dc
ResearcherID	J-6585-2016
Publons author ID	230545
SNSF person ID	wds:Q42583827-F6EB13A9-052C-4235-B18F-D0F6C62367F9
SNSF person ID	78409
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q42583827
is author of	ICSBP is essential for the development of mouse type I interferon-producing cells and for the generation and activation of CD8alpha(+) dendritic cells ICSBP is critically involved in the normal development and trafficking of Langerhans cells and dermal dendritic cells Cyclophosphamide synergizes with type I interferons through systemic dendritic cell reactivation and induction of immunogenic tumor apoptosis Type I interferons produced by dendritic cells promote their phenotypic and functional activation Classification of current anticancer immunotherapies ICSBP/IRF-8 differentially regulates antigen uptake during dendritic-cell development and affects antigen presentation to CD4+ T cells IL-15 is expressed by dendritic cells in response to type I IFN, double-stranded RNA, or lipopolysaccharide and promotes dendritic cell activation Combining Type I Interferons and 5-Aza-2'-Deoxycitidine to Improve Anti-Tumor Response against Melanoma The tumor microenvironment: a pitch for multiple players. Cyclophosphamide induces type I interferon and augments the number of CD44(hi) T lymphocytes in mice: implications for strategies of chemoimmunotherapy of cancer Cancer-driven dynamics of immune cells in a microfluidic environment. Type I IFNs control antigen retention and survival of CD8α(+) dendritic cells after uptake of tumor apoptotic cells leading to cross-priming STAT1 regulates IFN-alpha beta- and IFN-gamma-dependent control of infection with Chlamydia pneumoniae by nonhemopoietic cells. Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1. Type I Interferons as Stimulators of DC-Mediated Cross-Priming: Impact on Anti-Tumor Response Organs on chip approach: a tool to evaluate cancer -immune cells interactions A multidisciplinary study using in vivo tumor models and microfluidic cell-on-chip approach to explore the cross-talk between cancer and immune cells. Cross talk between cancer and immune cells: exploring complex dynamics in a microfluidic environment Detection of C-myb genetic alterations and mutant p53 serum protein in patients with benign and malignant colon lesions IRF-8 controls melanoma progression by regulating the cross talk between cancer and immune cells within the tumor microenvironment. Interferon regulatory factor 8-deficiency determines massive neutrophil recruitment but T cell defect in fast growing granulomas during tuberculosis Novel allergic asthma model demonstrates ST2-dependent dendritic cell targeting by cypress pollen Eosinophils: The unsung heroes in cancer? The Pleiotropic Immunomodulatory Functions of IL-33 and Its Implications in Tumor Immunity IL-33 restricts tumor growth and inhibits pulmonary metastasis in melanoma-bearing mice through eosinophils. Possible use of lymphoid CD subsets as prognostic markers for plasma cell dyscrasias Follow-up of IgD-κ multiple myeloma by monitoring free light chains and total heavy chain IgD: A case report Type I IFN regulate DC turnover in vivo. Mycobacterium tuberculosis PstS1 amplifies IFN-γ and induces IL-17/IL-22 responses by unrelated memory CD4+ T cells via dendritic cell activation Acidic microenvironment plays a key role in human melanoma progression through a sustained exosome mediated transfer of clinically relevant metastatic molecules

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