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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2007-11-27
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pubmed:abstractText |
We previously reported that joint swelling, synovial thickening, and cartilage matrix depletion induced by the injection of anti-collagen monoclonal antibodies and lipopolysaccharide (LPS) in BALB/c mice are increased in the absence of inhibitory leukocyte immunoglobulin (Ig)-like receptor B4 (LILRB4; formerly gp49B1) in a neutrophil-dependent manner. Because both mast cells and neutrophils express LILRB4, we sought a mast cell requirement with mast cell-deficient mouse strains, but unexpectedly obtained full arthritis in Kit(W-sh) mice and full resistance in Kit(W/KitW-v) mice. Kit(W-sh) mice were indeed mast cell deficient as assessed by histology and the absence of IgE/mast cell-dependent passive cutaneous anaphylaxis in the ear and joint as well as passive systemic anaphylaxis. Deletion of LILRB4 in Kit(W-sh) mice exacerbated anti-collagen/LPS-induced joint swelling that was abolished by neutrophil depletion, establishing a counterregulatory role for LILRB4 in the absence of mast cells. Whereas blood neutrophil levels and LPS-elicited tissue neutrophilia were equal in Kit(W-sh) and Kit+ mice, both were impaired in Kit(W/KitW-v) mice. Although both strains are mast cell deficient and protected from IgE-mediated anaphylactic reactions, their dramatically different responses to autoantibody-mediated, neutrophil-dependent immune complex arthritis suggest that other host differences determine the extent of mast cell involvement. Thus, a conclusion for an absolute mast cell role in a pathobiologic process requires evidence from both strains.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-10515869,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-1084999,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-11457897,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-11466382,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-11932261,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-12215644,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-14557414,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-14966572,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-15353554,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-1545120,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-15649271,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-15827966,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-16127161,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-16567386,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-16710480,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-16847336,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-16873664,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-1693331,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-1705866,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-17114491,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-17277081,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-17923505,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-5765776,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-7117838,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-7515715,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-7521281,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17998392-7537375
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1540-9538
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
26
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pubmed:volume |
204
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2797-802
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17998392-Animals,
pubmed-meshheading:17998392-Antibodies,
pubmed-meshheading:17998392-Arthritis, Experimental,
pubmed-meshheading:17998392-Collagen,
pubmed-meshheading:17998392-Joint Diseases,
pubmed-meshheading:17998392-Lipopolysaccharides,
pubmed-meshheading:17998392-Mast Cells,
pubmed-meshheading:17998392-Membrane Glycoproteins,
pubmed-meshheading:17998392-Mice,
pubmed-meshheading:17998392-Mice, Inbred BALB C,
pubmed-meshheading:17998392-Mice, Knockout,
pubmed-meshheading:17998392-Neutrophils,
pubmed-meshheading:17998392-Proto-Oncogene Proteins c-kit,
pubmed-meshheading:17998392-Receptors, Immunologic
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pubmed:year |
2007
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pubmed:articleTitle |
Mast cell deficiency in Kit(W-sh) mice does not impair antibody-mediated arthritis.
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pubmed:affiliation |
Department of Medicine, Harvard Medical School, and Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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