Linked Life Data

17785830

Source:http://linkedlifedata.com/resource/pubmed/id/17785830

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-9-5
pubmed:abstractText
Alternatively activated macrophages (AAMPhi) are found in abundance during chronic Th2 inflammatory responses to metazoan parasites. Important roles for these macrophages are being defined, particularly in the context of Th2-mediated pathology and fibrosis. However, a full understanding of the requirements for alternative activation, particularly at the innate level, is lacking. We present evidence that alternative activation by the Th2 cytokines IL-4 and IL-13 is an innate and rapid response to tissue injury that takes place even in the absence of an infectious agent. This early response does not require CD4+ Th2 cells because it occurred in RAG-deficient mice. However, class II-restricted CD4+ T cell help is essential to maintain AAMPhi in response to infection, because AAMPhi were absent in RAG-deficient and MHC class II-deficient, but not B cell-deficient mice after chronic exposure to the nematode parasite, Brugia malayi. The absence of AAMPhi was associated with increased neutrophilia and reduced eosinophilia, suggesting that AAMPhi are involved in the clearance of neutrophils as well as the recruitment of eosinophils. Consistent with this hypothesis, AAMPhi show enhanced phagocytosis of apoptotic neutrophils, but not latex beads. Our data demonstrate that alternative activation by type 2 cytokines is an innate response to injury that can occur in the absence of an adaptive response. However, analogous to classical activation by microbial pathogens, Th2 cells are required for maintenance and full activation during the ongoing response to metazoan parasites.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3926-36
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17785830-Animals, pubmed-meshheading:17785830-Arginase, pubmed-meshheading:17785830-Brugia malayi, pubmed-meshheading:17785830-CD4-Positive T-Lymphocytes, pubmed-meshheading:17785830-Cell Movement, pubmed-meshheading:17785830-Chronic Disease, pubmed-meshheading:17785830-Female, pubmed-meshheading:17785830-Filariasis, pubmed-meshheading:17785830-Immunity, Active, pubmed-meshheading:17785830-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:17785830-Lectins, pubmed-meshheading:17785830-Macrophage Activation, pubmed-meshheading:17785830-Male, pubmed-meshheading:17785830-Mice, pubmed-meshheading:17785830-Mice, Inbred C57BL, pubmed-meshheading:17785830-Mice, Knockout, pubmed-meshheading:17785830-Nerve Growth Factor, pubmed-meshheading:17785830-Neutrophils, pubmed-meshheading:17785830-Proteins, pubmed-meshheading:17785830-beta-N-Acetylhexosaminidases
pubmed:year
2007
pubmed:articleTitle
Alternative activation is an innate response to injury that requires CD4+ T cells to be sustained during chronic infection.
pubmed:affiliation
Tropical Disease Research Unit, University of California, San Francisco, CA 94143, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't