Linked Life Data

21257967

Source:http://linkedlifedata.com/resource/pubmed/id/21257967

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-2-17
pubmed:abstractText
Although many studies have shown that pulmonary surfactant protein (SP)-A functions in innate immunity, fewer studies have addressed its role in adaptive immunity and allergic hypersensitivity. We hypothesized that SP-A modulates the phenotype and prevalence of dendritic cells (DCs) and CD4(+) T cells to inhibit Th2-associated inflammatory indices associated with allergen-induced inflammation. In an OVA model of allergic hypersensitivity, SP-A(-/-) mice had greater eosinophilia, Th2-associated cytokine levels, and IgE levels compared with wild-type counterparts. Although both OVA-exposed groups had similar proportions of CD86(+) DCs and Foxp3(+) T regulatory cells, the SP-A(-/-) mice had elevated proportions of CD4(+) activated and effector memory T cells in their lungs compared with wild-type mice. Ex vivo recall stimulation of CD4(+) T cell pools demonstrated that cells from the SP-A(-/-) OVA mice had the greatest proliferative and IL-4-producing capacity, and this capability was attenuated with exogenous SP-A treatment. Additionally, tracking proliferation in vivo demonstrated that CD4(+) activated and effector memory T cells expanded to the greatest extent in the lungs of SP-A(-/-) OVA mice. Taken together, our data suggested that SP-A influences the prevalence, types, and functions of CD4(+) T cells in the lungs during allergic inflammation and that SP deficiency modifies the severity of inflammation in allergic hypersensitivity conditions like asthma.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
186
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2842-9
pubmed:meshHeading
pubmed-meshheading:21257967-Allergens, pubmed-meshheading:21257967-Animals, pubmed-meshheading:21257967-CD4-Positive T-Lymphocytes, pubmed-meshheading:21257967-Cell Proliferation, pubmed-meshheading:21257967-Dendritic Cells, pubmed-meshheading:21257967-Immunologic Memory, pubmed-meshheading:21257967-Immunophenotyping, pubmed-meshheading:21257967-Inflammation, pubmed-meshheading:21257967-Lung, pubmed-meshheading:21257967-Lymphocyte Activation, pubmed-meshheading:21257967-Mice, pubmed-meshheading:21257967-Mice, Inbred C57BL, pubmed-meshheading:21257967-Mice, Knockout, pubmed-meshheading:21257967-Ovalbumin, pubmed-meshheading:21257967-Pulmonary Surfactant-Associated Protein A, pubmed-meshheading:21257967-Respiratory Hypersensitivity, pubmed-meshheading:21257967-Severity of Illness Index, pubmed-meshheading:21257967-Th2 Cells
pubmed:year
2011
pubmed:articleTitle
Lung effector memory and activated CD4+ T cells display enhanced proliferation in surfactant protein A-deficient mice during allergen-mediated inflammation.
pubmed:affiliation
Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, N.I.H., Extramural