Linked Life Data

15067045

Source:http://linkedlifedata.com/resource/pubmed/id/15067045

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2004-4-6
pubmed:abstractText
Results from several mouse tolerance models indicate that autoreactive B cells in peripheral lymphoid organs develop an anergic phenotype, migrate to the boundary between the T cell zone and the B cell follicle (T/B boundary), and undergo rapid cell death. We have used B cells from mice that are double-transgenic for soluble hen egg lysozyme (HEL) and an Ig that recognizes HEL with a high affinity to characterize the mechanisms underlying the migration and elimination of autoreactive B cells. In contrast to the situation for acutely activated B cells, we find that anergic B cells have reduced levels of CXCR5, the receptor for the follicular chemokine, CXCL13, and this contributes to their exclusion from follicles. CCR7 expression is required for follicular exclusion of anergic cells, although up-regulation of the receptor does not appear to be necessary. By TUNEL analysis, we observe that excluded anergic cells die in situ at the T/B boundary. We also show that this elimination occurs via a Fas-independent mechanism. Using CCR7(-/-)Ig(HEL)-transgenic B cells we find that localization to the T/B boundary is not a necessary event to achieve the competitive elimination of autoantigen-binding B cells. These findings characterize the mechanism for follicular exclusion of autoantigen-binding B cells and they indicate that B cells compete for survival by mechanisms that are separate from competition for the follicular niche.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
172
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4700-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:15067045-Adoptive Transfer, pubmed-meshheading:15067045-Animals, pubmed-meshheading:15067045-Antigens, CD95, pubmed-meshheading:15067045-Autoantigens, pubmed-meshheading:15067045-B-Lymphocyte Subsets, pubmed-meshheading:15067045-Binding, Competitive, pubmed-meshheading:15067045-Cell Death, pubmed-meshheading:15067045-Cell Movement, pubmed-meshheading:15067045-Clonal Anergy, pubmed-meshheading:15067045-Interphase, pubmed-meshheading:15067045-Lymphocyte Activation, pubmed-meshheading:15067045-Lymphocyte Transfusion, pubmed-meshheading:15067045-Lymphoid Tissue, pubmed-meshheading:15067045-Mice, pubmed-meshheading:15067045-Mice, Inbred C57BL, pubmed-meshheading:15067045-Mice, Inbred MRL lpr, pubmed-meshheading:15067045-Mice, Knockout, pubmed-meshheading:15067045-Mice, Transgenic, pubmed-meshheading:15067045-Receptors, CCR7, pubmed-meshheading:15067045-Receptors, CXCR5, pubmed-meshheading:15067045-Receptors, Chemokine, pubmed-meshheading:15067045-Receptors, Cytokine, pubmed-meshheading:15067045-T-Lymphocyte Subsets
pubmed:year
2004
pubmed:articleTitle
Requirements for follicular exclusion and competitive elimination of autoantigen-binding B cells.
pubmed:affiliation
Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, CA 94143, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't