CDI and Gamma Delta+ in Viral Myocarditis View Homepage


Ontology type: schema:MonetaryGrant     


Grant Info

YEARS

1998-2007

FUNDING AMOUNT

871063 USD

ABSTRACT

DESCRIPTION (provided by applicant): Coxsackievirus B3 (CVB3) infection causes myocarditis and dilated cardiomyopathy. The pathogenic mechanisms of the disease are complex. Myocarditis susceptibility correlates with activation of T cells expressing the Vgamma4 T cell receptor (TCR), CD4+ Thi (IFNgamma+) and CD8+alphabeta TCR+ autoimmune cytolytic T cells (CTL). Myocarditis resistance correlates to activation of Vgamma1+ and CD4+Th2 (IL4+) cells, and the absence of autoimmune CD8+alphabeta TCR+ effectors. Vgamma4+ cells kill both CVB3-infected myocytes and CD4+Th2 cells in vitro, and comprise up to 50% of the inflammatory T cells in the heart. CD8+alphabeta TCR+ autoimmune CTL kill uninfected but not virus-infected myocytes, and are the second most populous inflammatory cells in myocarditis. Since both Vgamma4+ and CD8+alphabeta TCR+ cells are cytolytic to cardiac myocytes in vitro, either or both populations might contribute to cardiac injury in vivo. Vgamma4+ cells recognize CD1, a major histocompatibility complex (MHC) class I-like molecule which normally presents hydrophobic lipid or peptide antigens. The autoimmune CD8+alphabeta TCR+ cells recognize antigen presented by classical MHC class I molecules. The overall goal of this application is to define the relative contributions of Vgamma4+ and CD8+alphabeta TCR+ cells to myocarditis in vivo, and determine whether Vgamma4+ cells facilitate CD8+alphabeta TCR+ cell activation by promoting CD4+ Th1 cell responses. The Specific Aims are to: 1) determine the relative importance of Vgamma4+ cell mediated killing of myocytes or modulation of CD4+ cell phenotype and activation of CD8+alphabeta TCR+ CTL in myocarditis; 2) determine CD1d expression in pathogenic versus non-pathogenic CVB3 infections and the role for lipid or peptide antigens in the CD1d-restricted Vgamma4+ T cell response; and 3) determine whether Vgamma4+ cells kill CD4+Th2 cells through CD1 -restricted responses. More... »

URL

http://projectreporter.nih.gov/project_info_description.cfm?aid=6893997

Related SciGraph Publications

JSON-LD is the canonical representation for SciGraph data.

TIP: You can open this SciGraph record using an external JSON-LD service: JSON-LD Playground Google SDTT

[
  {
    "@context": "https://springernature.github.io/scigraph/jsonld/sgcontext.json", 
    "about": [
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/2211", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "type": "DefinedTerm"
      }
    ], 
    "amount": {
      "currency": "USD", 
      "type": "MonetaryAmount", 
      "value": "871063"
    }, 
    "description": "DESCRIPTION (provided by applicant): Coxsackievirus B3 (CVB3) infection causes myocarditis and dilated cardiomyopathy. The pathogenic mechanisms of the disease are complex. Myocarditis susceptibility correlates with activation of T cells expressing the Vgamma4 T cell receptor (TCR), CD4+ Thi (IFNgamma+) and CD8+alphabeta TCR+ autoimmune cytolytic T cells (CTL). Myocarditis resistance correlates to activation of Vgamma1+ and CD4+Th2 (IL4+) cells, and the absence of autoimmune CD8+alphabeta TCR+ effectors. Vgamma4+ cells kill both CVB3-infected myocytes and CD4+Th2 cells in vitro, and comprise up to 50% of the inflammatory T cells in the heart. CD8+alphabeta TCR+ autoimmune CTL kill uninfected but not virus-infected myocytes, and are the second most populous inflammatory cells in myocarditis. Since both Vgamma4+ and CD8+alphabeta TCR+ cells are cytolytic to cardiac myocytes in vitro, either or both populations might contribute to cardiac injury in vivo. Vgamma4+ cells recognize CD1, a major histocompatibility complex (MHC) class I-like molecule which normally presents hydrophobic lipid or peptide antigens. The autoimmune CD8+alphabeta TCR+ cells recognize antigen presented by classical MHC class I molecules. The overall goal of this application is to define the relative contributions of Vgamma4+ and CD8+alphabeta TCR+ cells to myocarditis in vivo, and determine whether Vgamma4+ cells facilitate CD8+alphabeta TCR+ cell activation by promoting CD4+ Th1 cell responses. The Specific Aims are to: 1) determine the relative importance of Vgamma4+ cell mediated killing of myocytes or modulation of CD4+ cell phenotype and activation of CD8+alphabeta TCR+ CTL in myocarditis; 2) determine CD1d expression in pathogenic versus non-pathogenic CVB3 infections and the role for lipid or peptide antigens in the CD1d-restricted Vgamma4+ T cell response; and 3) determine whether Vgamma4+ cells kill CD4+Th2 cells through CD1 -restricted responses.", 
    "endDate": "2007-06-30T00:00:00Z", 
    "funder": {
      "id": "https://www.grid.ac/institutes/grid.279885.9", 
      "type": "Organization"
    }, 
    "id": "sg:grant.2535946", 
    "identifier": [
      {
        "name": "dimensions_id", 
        "type": "PropertyValue", 
        "value": [
          "2535946"
        ]
      }, 
      {
        "name": "nih_id", 
        "type": "PropertyValue", 
        "value": [
          "R01HL058583"
        ]
      }
    ], 
    "inLanguage": [
      "en"
    ], 
    "keywords": [
      "gamma delta+", 
      "CD8+alphabeta TCR+ cell activation", 
      "CD4+ cell phenotype", 
      "non-pathogenic CVB3 infections", 
      "cardiomyopathy", 
      "IL4+", 
      "role", 
      "myocarditis susceptibility", 
      "peptide antigens", 
      "CD4+ Thi", 
      "cardiac injury", 
      "vitro", 
      "major histocompatibility complex", 
      "population", 
      "pathogenic mechanisms", 
      "class I", 
      "myocytes", 
      "hydrophobic lipids", 
      "absence", 
      "CD1d expression", 
      "applicants", 
      "CD8+alphabeta TCR+ CTL", 
      "killing", 
      "coxsackievirus B3", 
      "description", 
      "heart", 
      "CD4+TH2 cells", 
      "Vgamma4+ T cell response", 
      "CD8+alphabeta TCR+ cells", 
      "Vgamma4+ cells", 
      "CDI", 
      "specific aim", 
      "response", 
      "like molecules", 
      "cardiac myocytes", 
      "relative importance", 
      "virus", 
      "CD8+alphabeta TCR+ autoimmune CTL", 
      "classical MHC class I molecules", 
      "vivo", 
      "activation", 
      "populous inflammatory cells", 
      "CD4+Th2", 
      "CD1", 
      "CTL", 
      "myocarditis", 
      "CD1d", 
      "autoimmune CD8+alphabeta TCR+ cells", 
      "viral myocarditis", 
      "Myocarditis resistance", 
      "IFNgamma+", 
      "cells", 
      "modulation", 
      "application", 
      "disease", 
      "overall goal", 
      "CVB3-infected myocytes", 
      "Vgamma4", 
      "infection", 
      "relative contribution", 
      "TCR", 
      "autoimmune CD8+alphabeta TCR+ effectors", 
      "Vgamma1+", 
      "CD4+ Th1 cell responses", 
      "antigen"
    ], 
    "name": "CDI and Gamma Delta+ in Viral Myocarditis", 
    "recipient": [
      {
        "id": "https://www.grid.ac/institutes/grid.59062.38", 
        "type": "Organization"
      }, 
      {
        "affiliation": {
          "id": "https://www.grid.ac/institutes/grid.59062.38", 
          "name": "UNIVERSITY OF VERMONT &ST AGRIC COLLEGE", 
          "type": "Organization"
        }, 
        "familyName": "HUBER", 
        "givenName": "SALLY A.", 
        "id": "sg:person.0674307324.29", 
        "type": "Person"
      }, 
      {
        "member": "sg:person.0674307324.29", 
        "roleName": "PI", 
        "type": "Role"
      }
    ], 
    "sameAs": [
      "https://app.dimensions.ai/details/grant/grant.2535946"
    ], 
    "sdDataset": "grants", 
    "sdDatePublished": "2019-03-07T11:58", 
    "sdLicense": "https://scigraph.springernature.com/explorer/license/", 
    "sdPublisher": {
      "name": "Springer Nature - SN SciGraph project", 
      "type": "Organization"
    }, 
    "sdSource": "s3://com.uberresearch.data.processor/core_data/20181219_192338/projects/base/nih_projects_10.xml.gz", 
    "startDate": "1998-04-01T00:00:00Z", 
    "type": "MonetaryGrant", 
    "url": "http://projectreporter.nih.gov/project_info_description.cfm?aid=6893997"
  }
]
 

Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

JSON-LD is a popular format for linked data which is fully compatible with JSON.

curl -H 'Accept: application/ld+json' 'https://scigraph.springernature.com/grant.2535946'

N-Triples is a line-based linked data format ideal for batch operations.

curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/grant.2535946'

Turtle is a human-readable linked data format.

curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/grant.2535946'

RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/grant.2535946'


 

This table displays all metadata directly associated to this object as RDF triples.

109 TRIPLES      19 PREDICATES      87 URIs      79 LITERALS      5 BLANK NODES

Subject Predicate Object
1 sg:grant.2535946 schema:about anzsrc-for:2211
2 schema:amount N4c7289390470411b9dbf0d47e85e876f
3 schema:description DESCRIPTION (provided by applicant): Coxsackievirus B3 (CVB3) infection causes myocarditis and dilated cardiomyopathy. The pathogenic mechanisms of the disease are complex. Myocarditis susceptibility correlates with activation of T cells expressing the Vgamma4 T cell receptor (TCR), CD4+ Thi (IFNgamma+) and CD8+alphabeta TCR+ autoimmune cytolytic T cells (CTL). Myocarditis resistance correlates to activation of Vgamma1+ and CD4+Th2 (IL4+) cells, and the absence of autoimmune CD8+alphabeta TCR+ effectors. Vgamma4+ cells kill both CVB3-infected myocytes and CD4+Th2 cells in vitro, and comprise up to 50% of the inflammatory T cells in the heart. CD8+alphabeta TCR+ autoimmune CTL kill uninfected but not virus-infected myocytes, and are the second most populous inflammatory cells in myocarditis. Since both Vgamma4+ and CD8+alphabeta TCR+ cells are cytolytic to cardiac myocytes in vitro, either or both populations might contribute to cardiac injury in vivo. Vgamma4+ cells recognize CD1, a major histocompatibility complex (MHC) class I-like molecule which normally presents hydrophobic lipid or peptide antigens. The autoimmune CD8+alphabeta TCR+ cells recognize antigen presented by classical MHC class I molecules. The overall goal of this application is to define the relative contributions of Vgamma4+ and CD8+alphabeta TCR+ cells to myocarditis in vivo, and determine whether Vgamma4+ cells facilitate CD8+alphabeta TCR+ cell activation by promoting CD4+ Th1 cell responses. The Specific Aims are to: 1) determine the relative importance of Vgamma4+ cell mediated killing of myocytes or modulation of CD4+ cell phenotype and activation of CD8+alphabeta TCR+ CTL in myocarditis; 2) determine CD1d expression in pathogenic versus non-pathogenic CVB3 infections and the role for lipid or peptide antigens in the CD1d-restricted Vgamma4+ T cell response; and 3) determine whether Vgamma4+ cells kill CD4+Th2 cells through CD1 -restricted responses.
4 schema:endDate 2007-06-30T00:00:00Z
5 schema:funder https://www.grid.ac/institutes/grid.279885.9
6 schema:identifier N28722a23ff134a81ab734e3b7aff5809
7 Ndd97e42a0fc64942acd4e7080f13d86b
8 schema:inLanguage en
9 schema:keywords CD1
10 CD1d
11 CD1d expression
12 CD4+ Th1 cell responses
13 CD4+ Thi
14 CD4+ cell phenotype
15 CD4+TH2 cells
16 CD4+Th2
17 CD8+alphabeta TCR+ CTL
18 CD8+alphabeta TCR+ autoimmune CTL
19 CD8+alphabeta TCR+ cell activation
20 CD8+alphabeta TCR+ cells
21 CDI
22 CTL
23 CVB3-infected myocytes
24 IFNgamma+
25 IL4+
26 Myocarditis resistance
27 TCR
28 Vgamma1+
29 Vgamma4
30 Vgamma4+ T cell response
31 Vgamma4+ cells
32 absence
33 activation
34 antigen
35 applicants
36 application
37 autoimmune CD8+alphabeta TCR+ cells
38 autoimmune CD8+alphabeta TCR+ effectors
39 cardiac injury
40 cardiac myocytes
41 cardiomyopathy
42 cells
43 class I
44 classical MHC class I molecules
45 coxsackievirus B3
46 description
47 disease
48 gamma delta+
49 heart
50 hydrophobic lipids
51 infection
52 killing
53 like molecules
54 major histocompatibility complex
55 modulation
56 myocarditis
57 myocarditis susceptibility
58 myocytes
59 non-pathogenic CVB3 infections
60 overall goal
61 pathogenic mechanisms
62 peptide antigens
63 population
64 populous inflammatory cells
65 relative contribution
66 relative importance
67 response
68 role
69 specific aim
70 viral myocarditis
71 virus
72 vitro
73 vivo
74 schema:name CDI and Gamma Delta+ in Viral Myocarditis
75 schema:recipient Ncc841750b7b5479baf3b79452e95184b
76 sg:person.0674307324.29
77 https://www.grid.ac/institutes/grid.59062.38
78 schema:sameAs https://app.dimensions.ai/details/grant/grant.2535946
79 schema:sdDatePublished 2019-03-07T11:58
80 schema:sdLicense https://scigraph.springernature.com/explorer/license/
81 schema:sdPublisher N1c9dcf4c77e64cafae2aca3f52122e8f
82 schema:startDate 1998-04-01T00:00:00Z
83 schema:url http://projectreporter.nih.gov/project_info_description.cfm?aid=6893997
84 sgo:license sg:explorer/license/
85 sgo:sdDataset grants
86 rdf:type schema:MonetaryGrant
87 N1c9dcf4c77e64cafae2aca3f52122e8f schema:name Springer Nature - SN SciGraph project
88 rdf:type schema:Organization
89 N28722a23ff134a81ab734e3b7aff5809 schema:name nih_id
90 schema:value R01HL058583
91 rdf:type schema:PropertyValue
92 N4c7289390470411b9dbf0d47e85e876f schema:currency USD
93 schema:value 871063
94 rdf:type schema:MonetaryAmount
95 Ncc841750b7b5479baf3b79452e95184b schema:member sg:person.0674307324.29
96 schema:roleName PI
97 rdf:type schema:Role
98 Ndd97e42a0fc64942acd4e7080f13d86b schema:name dimensions_id
99 schema:value 2535946
100 rdf:type schema:PropertyValue
101 anzsrc-for:2211 schema:inDefinedTermSet anzsrc-for:
102 rdf:type schema:DefinedTerm
103 sg:person.0674307324.29 schema:affiliation https://www.grid.ac/institutes/grid.59062.38
104 schema:familyName HUBER
105 schema:givenName SALLY A.
106 rdf:type schema:Person
107 https://www.grid.ac/institutes/grid.279885.9 schema:Organization
108 https://www.grid.ac/institutes/grid.59062.38 schema:name UNIVERSITY OF VERMONT &ST AGRIC COLLEGE
109 rdf:type schema:Organization
 




Preview window. Press ESC to close (or click here)


...