Linked Life Data

19573259

Source:http://linkedlifedata.com/resource/pubmed/id/19573259

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2009-8-11
pubmed:abstractText
The outcome of Plasmodium yoelii 17XL-infected BALB/c and DBA/2 mice, ranging from death to spontaneous cure, respectively, depends largely on the establishment of effective pro-inflammatory type 1 responses during the early stages of infection and associates with CD4(+)CD25(+)Foxp3(+)regulatory T cells (Tregs). Here, effects of Tregs were analysed on early P. yoelii 17XL infection in BALB/c and DBA/2 mice. In vivo depletion of Tregs significantly reversed the inhibited establishment of effective pro-inflammatory type 1 responses in BALB/c mice, indicating that this cell population contributed to the suppression of T-cell function in malaria. Moreover, the proportion and absolute numbers of IL-10-secreting Tregs in BALB/c mice were significantly higher than that found in DBA/2 mice by intracytoplasmic staining, and IL-10 production was correlated with the Tregs population. In addition, in vivo Tregs depletion decreased the production of IL-10 and the apoptosis of CD4+ T cells. Consistently, IL-10R blockade also had the same effect as that of Tregs depletion in P. yoelii 17XL-infected BALB/c mice. Our data demonstrate that Tregs perhaps have an important role in regulating pro-inflammatory type 1 responses in an IL-10-dependent manner and induce CD4+ T cell apoptosis during the early stage of P. yoelii 17XL infection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1469-8161
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
136
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1107-20
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Effects of CD4(+)CD25(+)Foxp3(+)regulatory T cells on early Plasmodium yoelii 17XL infection in BALB/c mice.
pubmed:affiliation
Department of Immunology, College of Basic Medical Sciences, China Medical University, Heping District, Shenyang, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't