Source:http://linkedlifedata.com/resource/pubmed/id/11441111
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
2001-7-6
|
| pubmed:abstractText |
We induced the passive reverse Arthus reaction to IgG immune complexes (IC) at different tissue sites in mice lacking C3 treated or not with a C5aR-specific antagonist, or in mice lacking mast cells (Kit(W)/Kit(W-v) mice), and compared the inflammatory responses with those in the corresponding wild-type mice. We confirmed that IC inflammation of skin can be mediated largely by mast cells expressing C5aR and FcgammaRIII. In addition, we provided evidence for C3-independent C5aR triggering, which may explain why the cutaneous Arthus reaction develops normally in C3(-/-) mice. Furthermore, some, but not all, of the acute changes associated with the Arthus response in the lung were significantly more intense in normal mice than in C3(-/-) or Kit(W)/Kit(W-v) mice, indicating for C3- and mast cell-dependent and -independent components. Finally, we demonstrated that C3 contributed to the elicitation of neutrophils to alveoli, which corresponded to an increased synthesis of TNF-alpha, macrophage-inflammatory protein-2, and cytokine-induced neutrophil chemoattractant. While mast cells similarly influenced alveolar polymorphonuclear leukocyte influx, the levels of these cytokines remained largely unaffected in mast cell deficiency. Together, the phenotypes of C3(-/-) mice and Kit(W)/Kit(W-v) mice suggest that complement and mast cells have distinct tissue site-specific requirements acting by apparently distinct mechanisms in the initiation of IC inflammation.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C5a,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Anaphylatoxin C5a,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
167
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1022-7
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:11441111-Animals,
pubmed-meshheading:11441111-Antigens, CD,
pubmed-meshheading:11441111-Arthus Reaction,
pubmed-meshheading:11441111-Cell Movement,
pubmed-meshheading:11441111-Complement C3,
pubmed-meshheading:11441111-Complement C5a,
pubmed-meshheading:11441111-Cytokines,
pubmed-meshheading:11441111-Immune Complex Diseases,
pubmed-meshheading:11441111-Immunoglobulin G,
pubmed-meshheading:11441111-Lung,
pubmed-meshheading:11441111-Male,
pubmed-meshheading:11441111-Mast Cells,
pubmed-meshheading:11441111-Mice,
pubmed-meshheading:11441111-Mice, Inbred C57BL,
pubmed-meshheading:11441111-Mice, Knockout,
pubmed-meshheading:11441111-Mice, Mutant Strains,
pubmed-meshheading:11441111-Neutrophils,
pubmed-meshheading:11441111-Organ Specificity,
pubmed-meshheading:11441111-Receptor, Anaphylatoxin C5a,
pubmed-meshheading:11441111-Receptors, Complement,
pubmed-meshheading:11441111-Skin
|
| pubmed:year |
2001
|
| pubmed:articleTitle |
Distinct tissue site-specific requirements of mast cells and complement components C3/C5a receptor in IgG immune complex-induced injury of skin and lung.
|
| pubmed:affiliation |
Department of Clinical Immunology, Medical School Hannover, 30625 Hannover, Germany.
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| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|