Source:http://linkedlifedata.com/resource/pubmed/id/12753808
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2003-5-19
|
| pubmed:abstractText |
Accumulating evidence indicates that the type IIB Fc receptor for IgG (FcgammaRIIB) plays a pivotal role in maintaining peripheral tolerance by suppressing excessive humoral and cellular immune responses. However, little is known about the mechanism by which the autoreactive B cells develop in the periphery in FcgammaRIIB-deficient mice. To clarify the role of FcgammaRIIB in the emergence of autoreactive B cells, we analyzed B-cell compartments in the autoimmune arthritis-susceptible DBA/1 mice devoid of FcgammaRIIB (DBA.IIB-/-) during the induction of collagen-induced arthritis (CIA). We found that DBA.IIB-/- showed an increase in the number of peripheral immature type 2 transitional (T2) B cells after immunization with type II collagen (C-II), followed by the enhanced severity of CIA with higher autoantibody titers to mouse C-II than those of wild-type DBA/1. In addition, elevated secretion of IL-1alpha by peritoneal macrophages from DBA.IIB-/- on stimulation with IgG immune complexes in vitro suggested the augmented effector cell responses in the CIA course of DBA.IIB-/-. These findings suggest that the FcgammaRIIB-dependent triple regulation in the peripheral T2 B cells, in the antibody production, and in the effector cell responses is crucial for suppressing CIA.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Fc gamma receptor IIB,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgG
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
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| pubmed:issn |
0896-8411
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
20
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
227-36
|
| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:12753808-Animals,
pubmed-meshheading:12753808-Antigens, CD,
pubmed-meshheading:12753808-Apoptosis,
pubmed-meshheading:12753808-Arthritis, Experimental,
pubmed-meshheading:12753808-Autoantibodies,
pubmed-meshheading:12753808-Autoimmunity,
pubmed-meshheading:12753808-B-Lymphocyte Subsets,
pubmed-meshheading:12753808-Cell Differentiation,
pubmed-meshheading:12753808-Collagen Type II,
pubmed-meshheading:12753808-Germinal Center,
pubmed-meshheading:12753808-Immunity, Cellular,
pubmed-meshheading:12753808-Interleukin-1,
pubmed-meshheading:12753808-Male,
pubmed-meshheading:12753808-Mice,
pubmed-meshheading:12753808-Mice, Inbred DBA,
pubmed-meshheading:12753808-Mice, Knockout,
pubmed-meshheading:12753808-Receptors, IgG,
pubmed-meshheading:12753808-Self Tolerance
|
| pubmed:year |
2003
|
| pubmed:articleTitle |
Deregulation of peripheral B-cell development in enhanced severity of collagen-induced arthritis in FcgammaRIIB-deficient mice.
|
| pubmed:affiliation |
Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Seiryo-machi 4-1, Sendai 980-8575, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|