About: Thomas Calzascia

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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	ikertzailea (eu) researcher (en) 연구원 (ko) 研究者 (ja) araştırmacı (tr) wetenschapper (nl) дослідник (uk) эрдэмтэн (mn) वैज्ञानिक (hi) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy)
rdfs:label	T Calzascia (es) T Calzascia (nl) T Calzascia (ast) Thomas Calzascia (en)
skos:prefLabel	T Calzascia (es) T Calzascia (nl) T Calzascia (ast) Thomas Calzascia (en)
name	T Calzascia (es) T Calzascia (nl) T Calzascia (ast) Thomas Calzascia (en)
given name	wds:Q56640562-2D4CFFB6-E5D7-4142-9F8C-D0D710C41F90
given name	Thomas
instance of	wds:Q56640562-50E7EF48-64DF-4B85-B43A-81CEFBA615E6
instance of	Homo sapiens
occupation	wds:Q56640562-E84BBF50-343A-49FD-987E-E48A86D62E3A
sex or gender	wds:Q56640562-5C055071-5474-4527-A989-BA2725CB4E38
educated at	wds:Q56640562-1F18A783-BC5C-4457-AB7B-048085A5A8AA wds:Q56640562-35535F0B-07F6-4793-8335-4A83C5C11186 wds:Q56640562-434F11CA-71BB-47A3-AD2C-BCE36260A4CC wds:Q56640562-CC960DA5-28F1-4858-8E8D-19AB3E4F32FF
occupation	researcher
sex or gender	male
educated at	University of Geneva
ORCID iD	wds:Q56640562-1F115BFF-F840-42D9-9BDD-6CF56FE4210A
ORCID iD	https://orcid.org/0000-0001-8225-6744
ORCID iD	0000-0001-8225-6744
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q56640562
is author of	Adjuvant IL-7 antagonizes multiple cellular and molecular inhibitory networks to enhance immunotherapies. IL-7 Engages Multiple Mechanisms to Overcome Chronic Viral Infection and Limit Organ Pathology Loss of the signaling adaptor TRAF1 causes CD8+ T cell dysregulation during human and murine chronic infection The brain parenchyma is permissive for full antitumor CTL effector function, even in the absence of CD4 T cells Deficiency of MALT1 paracaspase activity results in unbalanced regulatory and effector T and B cell responses leading to multiorgan inflammation Homing phenotypes of tumor-specific CD8 T cells are predetermined at the tumor site by crosspresenting APCs. Cutting edge: cross-presentation as a mechanism for efficient recruitment of tumor-specific CTL to the brain. Loss of Fas (CD95/APO-1) expression by antigen-specific cytotoxic T cells is reversed by inhibiting DNA methylation. Aggravation of viral hepatitis by platelet-derived serotonin A Critical Role for the Innate Immune Signaling Molecule IRAK-4 in T Cell Activation CD4 T cells, lymphopenia, and IL-7 in a multistep pathway to autoimmunity TNF-alpha is critical for antitumor but not antiviral T cell immunity in mice Lentiviral transduction of dendritic cells confers protective antiviral immunity in vivo IRAK-4 kinase activity is required for IRAK-4-dependent innate and adaptive immune responses. Two Antagonistic MALT1 Auto-Cleavage Mechanisms Reveal a Role for TRAF6 to Unleash MALT1 Activation Partial deficiency of sphingosine-1-phosphate lyase confers protection in experimental autoimmune encephalomyelitis Improved cancer immunotherapy by a CD25-mimobody conferring selectivity to human interleukin-2. Highly reduced binding to high and low affinity mouse Fc gamma receptors by L234A/L235A and N297A Fc mutations engineered into mouse IgG2a T-cell immune responses in the brain and their relevance for cerebral malignancies The T-cell fingerprint of MALT1 paracaspase revealed by selective inhibition. Peripheral tolerance limits CNS accumulation of CD8 T cells specific for an antigen shared by tumor cells and normal astrocytes. Selective MALT1 paracaspase inhibition does not block TNF-α production downstream of TLR4 in myeloid cells. Exposure to sequestered self-antigens in vivo is not sufficient for the induction of autoimmune diabetes Vav1 GEF activity is required for T cell mediated allograft rejection Efficient induction of CD8 T-associated immune protection by vaccination with mRNA transfected dendritic cells Malt1 Protease Deficiency in Mice Disrupts Immune Homeostasis at Environmental Barriers and Drives Systemic T Cell-Mediated Autoimmunity
is author of	wds:Q36121743-3D66F34E-F89E-40C9-B710-563201CE95F1 wds:Q36239551-0B4812C3-3853-486C-9764-1F6A843D6675 wds:Q39141421-40F34A99-AB2D-47D4-B604-A8D40AFB5BDB wds:Q38934502-5C5797E5-455B-4753-9698-019C4061F913 wds:Q50099722-C0082C6F-EBE7-4056-B9DD-4373ECB60579 wds:Q61727556-1E3BC196-81E3-4DA2-9D60-C0F0DC8D66C3 wds:Q57949127-913C1541-48E3-4EBB-A37A-9E099863D31D wds:Q74279859-8B1E93F1-3378-4248-B7DC-6508D99D1C9E wds:Q35679587-9D842252-7610-4272-B8C2-FEF831E6CB0C wds:Q36296891-671A4C27-6171-444A-98C8-8A790EE97D4E wds:Q47936492-936709AD-2752-4636-BF9D-90901562685E wds:Q73371191-A6FDD763-0BC0-4590-A435-08FCD7CD1669 wds:Q44528411-F4FFEE7A-7859-493A-9AE6-D25F0A9C3CA7 wds:Q48222103-079BC285-FEFC-46EC-9CB1-BBDCC67C0BF4 wds:Q79315640-E489B25F-7182-41D7-8E86-CB5F0F85C9FA wds:Q45218233-14088CF2-8789-42C7-B83D-6AEE3EE330AF wds:Q39356027-8518F28C-1AF9-4464-8BBB-4B82FF7F0AFB wds:Q54022680-0F4404A5-E21F-4F03-8412-F0F9C954477E wds:Q36361262-55EE7AB5-3774-4AD8-A541-6C5B00CD02FA wds:Q41240873-C606A119-334E-44AB-B085-A391E46C1DA8 wds:Q49852317-1597AB2C-F7BE-4291-8AA6-D578004B91CE wds:Q90974282-DA3CD8AB-38BD-4FC2-B11F-2F4C7EB813C3 wds:Q35122548-BA36438E-7C85-469A-A4BF-D624A3ABABD0 wds:Q36498454-6209C3E8-C77A-40D5-911D-7D002CAFD49A wds:Q40455900-3F657B22-8D25-4890-99B3-DA77A37F40F7 wds:Q55466316-EEDE77C9-2394-48E0-8EC2-1D7868ED978F

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