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Direct T helper-B cell interactions induce an early B cell activation antigen

We have explored the consequences for the B cell of cognate interaction with T cells. Early expression of the B cell-restricted cell surface activation antigen, BLAST-2, has been used as an assay system to measure direct T-B cell collaboration. BLAST-2 is preferentially expressed by allogenic B cell...

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Detalles Bibliográficos
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1986
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2188453/
https://www.ncbi.nlm.nih.gov/pubmed/2945893
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description We have explored the consequences for the B cell of cognate interaction with T cells. Early expression of the B cell-restricted cell surface activation antigen, BLAST-2, has been used as an assay system to measure direct T-B cell collaboration. BLAST-2 is preferentially expressed by allogenic B cells cultured with MHC class II antigen- restricted Th clone cells matched to the DR specificity of the target B cells. B cells cultured with DR-mismatched allospecific Th cells express minimal BLAST-2. Th cell-induced BLAST-2 expression appears to be accessory cell independent and occurs as early as 8 h after initiation of culture, with peak expression at 18 h. Direct T-B cell contact, rather than Th-derived lymphokines, provides the most efficient stimulus for BLAST-2 expression. Crosslinking of sIg on B cells is a poor stimulus for BLAST-2 expression. The BLAST-2 assay permits the evaluation of early events associated with B cell activation through cognate interactions, and may facilitate subsequent studies of the mechanism of B cell differentiation.
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spelling pubmed-21884532008-04-17 Direct T helper-B cell interactions induce an early B cell activation antigen J Exp Med Articles We have explored the consequences for the B cell of cognate interaction with T cells. Early expression of the B cell-restricted cell surface activation antigen, BLAST-2, has been used as an assay system to measure direct T-B cell collaboration. BLAST-2 is preferentially expressed by allogenic B cells cultured with MHC class II antigen- restricted Th clone cells matched to the DR specificity of the target B cells. B cells cultured with DR-mismatched allospecific Th cells express minimal BLAST-2. Th cell-induced BLAST-2 expression appears to be accessory cell independent and occurs as early as 8 h after initiation of culture, with peak expression at 18 h. Direct T-B cell contact, rather than Th-derived lymphokines, provides the most efficient stimulus for BLAST-2 expression. Crosslinking of sIg on B cells is a poor stimulus for BLAST-2 expression. The BLAST-2 assay permits the evaluation of early events associated with B cell activation through cognate interactions, and may facilitate subsequent studies of the mechanism of B cell differentiation. The Rockefeller University Press 1986-11-01 /pmc/articles/PMC2188453/ /pubmed/2945893 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Direct T helper-B cell interactions induce an early B cell activation antigen
title Direct T helper-B cell interactions induce an early B cell activation antigen
title_full Direct T helper-B cell interactions induce an early B cell activation antigen
title_fullStr Direct T helper-B cell interactions induce an early B cell activation antigen
title_full_unstemmed Direct T helper-B cell interactions induce an early B cell activation antigen
title_short Direct T helper-B cell interactions induce an early B cell activation antigen
title_sort direct t helper-b cell interactions induce an early b cell activation antigen
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2188453/
https://www.ncbi.nlm.nih.gov/pubmed/2945893