Linked Life Data

17689290

Source:http://linkedlifedata.com/resource/pubmed/id/17689290

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2007-9-17
pubmed:abstractText
The mechanisms underlying the failure to control the growth and systemic spread of Leishmania parasites in human visceral leishmaniasis (VL) are not well understood. Although the absence of antigen-specific Th1 responses in the peripheral blood mononuclear cells from VL patients is thought to be causally related to disease progression, the finding that these patients also express elevated interferon-gamma mRNA in lesional tissue, as well as elevated serum levels of proinflammatory cytokines, suggests that their immunological defect cannot be explained simply by immune tolerance or Th2 polarization. As a possible homeostatic mechanism to control persistent infection-induced inflammation, elevated levels of the regulatory cytokine interleukin (IL)-10 have been reported repeatedly in clinical studies of VL. Here, we review the studies with relevance to immune responses in human VL and highlight the central role that IL-10 might have in the pathogenesis of VL and as a target for immune-based therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1471-4906
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
378-84
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Interleukin-10 and the pathogenesis of human visceral leishmaniasis.
pubmed:affiliation
Laboratory of Parasitic Diseases, Bldg 4 RmB1-12, National Institute of Allergy and Infectious Diseases, 4 Center Drive MSC0425, Bethesda, MD 20892-0425, USA.
pubmed:publicationType
Journal Article, Review