| pubmed-article:20038598 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20038598 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:20038598 | lifeskim:mentions | umls-concept:C0003320 | lld:lifeskim |
| pubmed-article:20038598 | lifeskim:mentions | umls-concept:C0020964 | lld:lifeskim |
| pubmed-article:20038598 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
| pubmed-article:20038598 | lifeskim:mentions | umls-concept:C1332708 | lld:lifeskim |
| pubmed-article:20038598 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
| pubmed-article:20038598 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:20038598 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:20038598 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:20038598 | pubmed:dateCreated | 2010-1-19 | lld:pubmed |
| pubmed-article:20038598 | pubmed:abstractText | Autoreactive B lymphocytes first encountering self-antigens in peripheral tissues are normally regulated by induction of anergy or apoptosis. According to the "two-signal" model, antigen recognition alone should render B cells tolerant unless T cell help or inflammatory signals such as lipopolysaccharide are provided. However, no such signals seem necessary for responses to T-independent type 2 (TI-2) antigens, which are multimeric antigens lacking T cell epitopes and Toll-like receptor ligands. How then do mature B cells avoid making a TI-2-like response to multimeric self-antigens? We present evidence that TI-2 antigens decorated with ligands of inhibitory sialic acid-binding Ig-like lectins (siglecs) are poorly immunogenic and can induce tolerance to subsequent challenge with immunogenic antigen. Two siglecs, CD22 and Siglec-G, contributed to tolerance induction, preventing plasma cell differentiation or survival. Although mutations in CD22 and its signaling machinery have been associated with dysregulated B cell development and autoantibody production, previous analyses failed to identify a tolerance defect in antigen-specific mutant B cells. Our results support a role for siglecs in B cell self-/nonself-discrimination, namely suppressing responses to self-associated antigens while permitting rapid "missing self"-responses to unsialylated multimeric antigens. The results suggest use of siglec ligand antigen constructs as an approach for inducing tolerance. | lld:pubmed |
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| pubmed-article:20038598 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20038598 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20038598 | pubmed:citationSubset | IM | lld:pubmed |
