Linked Life Data

19482700

Source:http://linkedlifedata.com/resource/pubmed/id/19482700

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2009-6-1
pubmed:abstractText
Candida albicans is the predominant cause of both superficial and invasive forms of candidosis, although the proportion of serious infections attributed to other members of the genus is rising.. The spectrum of host defences include cell mediated immunity which is comprised of cytokine release by lymphocytes and activation of natural killer cells and lymphocytes by interleukins.. An increasing body of evidence supports a role for specific antibody in protection against invasive Candida infection. Clinical observations indicate that mucocutaneous Candida infections are commonly associated with defective cell-mediated immune responses. Innate immunity is the dominant protective mechanism against disseminated candidosis. Quantitative and qualitative abnormalities of neutrophils and monocytes are associated with systemic candidosis. In the present review virulence factors and the spectrum of immune responses are discussed in relation to the perspective for the development of appropriate vaccines against Candida. Here we present an overview of toll-like receptor signalling, cellular-dependent responses, the role of specific antibodies in protection against Candida, and the array of immune mechanisms that operate in gastrointestinal, vaginal and oral candidosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1945-0524
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
246-57
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
How the host fights against Candida infections.
pubmed:affiliation
Department of Bacteriology and Immunology, University of Helsinki, Finland. Malcolm.richardson@helsinki.fi
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't