Linked Life Data

19750483

Source:http://linkedlifedata.com/resource/pubmed/id/19750483

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2010-1-27
pubmed:abstractText
Here, we show that Treg limit intestinal pathology during nematode infection and that they control the onset and magnitude of the anti-parasitic Th Th2 response. Using mice expressing the diphtheria toxin receptor under the control of the foxp3 locus, we removed Foxp3(+) Treg during the early phase of infection with Heligmosomoides polygyrus bakeri. Depletion of Treg in infected animals did not affect adult worm burden, but led to increased pathology at the site of infection. Infected, depleted mice displayed higher frequencies of activated CD4(+) T cells and increased levels of the Th2 cytokines IL-4 and IL-13. The stronger parasite-specific Th2 response was accompanied by higher levels of IL-10. Only a moderate change in Th1 (IFN-gamma) reactivity was detected in worm-infected, Treg-depleted mice. Furthermore, we detected an accelerated onset of parasite-specific Th2 and IL-10 responses in the transient absence of Foxp3(+) Treg. However, adult worm burdens were not affected by the increased Th2-reactivity in Treg-depleted mice. Hence, our data show that Treg restrict the onset and strength of Th2 responses during intestinal worm infection, while increasing primary Th2 responses does not necessarily lead to killing of larvae or accelerated expulsion of adult worms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1521-4141
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3066-77
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Establishment of nematode infection despite increased Th2 responses and immunopathology after selective depletion of Foxp3+ cells.
pubmed:affiliation
Department of Molecular Parasitology, Humboldt-University of Berlin, Berlin, Germany. sebastian.rausch@hu-berlin.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't