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Lyb-2 system of mouse B cells. Evidence for a role in the generation of antibody-forming cells
The Lyb-2 cell-surface alloantigens of the mouse are selectively and perhaps exclusively expressed in the B lymphocyte lineage, but not on antibody- forming cells. Thus if the Lyb-2 molecule is concerned in specific B cell function, it must participate in the generative phase of the antibody respons...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
1981
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186058/ https://www.ncbi.nlm.nih.gov/pubmed/6969779 |
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author | Yakura, H Shen, F-W Kaemmer, M Boyse, EA |
author_facet | Yakura, H Shen, F-W Kaemmer, M Boyse, EA |
author_sort | Yakura, H |
collection | PubMed |
description | The Lyb-2 cell-surface alloantigens of the mouse are selectively and perhaps exclusively expressed in the B lymphocyte lineage, but not on antibody- forming cells. Thus if the Lyb-2 molecule is concerned in specific B cell function, it must participate in the generative phase of the antibody response. Accordingly, monoclonal Lyb-2 antibody was found to depress the plaque- forming cell (PFC) response to sheep erythrocytes in 5-d Mishell-Dutton assays when added within the first 3 d of culture, but not later. The rate of PFC generation was not affected, signifying an absolute reduction in the number of PFC generated. Because reduction of PFC counts by Lyb-2 antibody was not affected by exclusion of Lyt-2(+) T cells, it is unlikely that the reduction depends on augmented suppression by T cells. Augmented B cell- mediated suppression is also unlikely, because the PFC response of serial combinations of congenic Lyb-2.1 and Lyb-2.2 cells, in the presence of monoclonal Lyb-2.1 antibody, was reduced only in direct proportion to the number of Lyb-2.1 cells present. The PFC response of Lyb-2.1/Lyb-2.2 heterozygous cells was not reduced by Lyb-2.1 antibody, presumably because generation of PFC is impeded only if most Lyb-2 sites are blocked. Further evidence that the molecule identified by Lyb-2 plays a critical role in the generation of antibody-forming cells (AFC) in response to T-dependent antigen comes from the finding that Lyb-2 antibody does not reduce the PFC response to the T-independent antigens trinitrophenylated (TNP) Brucella abortus and TNP-FicolI, although elimination of Lyb-2(+) cells from the starting population by Lyb-2 antibody and complement reduces the PFC response to T- dependent and T-independent antigens alike. |
format | Text |
id | pubmed-2186058 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1981 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21860582008-04-17 Lyb-2 system of mouse B cells. Evidence for a role in the generation of antibody-forming cells Yakura, H Shen, F-W Kaemmer, M Boyse, EA J Exp Med Articles The Lyb-2 cell-surface alloantigens of the mouse are selectively and perhaps exclusively expressed in the B lymphocyte lineage, but not on antibody- forming cells. Thus if the Lyb-2 molecule is concerned in specific B cell function, it must participate in the generative phase of the antibody response. Accordingly, monoclonal Lyb-2 antibody was found to depress the plaque- forming cell (PFC) response to sheep erythrocytes in 5-d Mishell-Dutton assays when added within the first 3 d of culture, but not later. The rate of PFC generation was not affected, signifying an absolute reduction in the number of PFC generated. Because reduction of PFC counts by Lyb-2 antibody was not affected by exclusion of Lyt-2(+) T cells, it is unlikely that the reduction depends on augmented suppression by T cells. Augmented B cell- mediated suppression is also unlikely, because the PFC response of serial combinations of congenic Lyb-2.1 and Lyb-2.2 cells, in the presence of monoclonal Lyb-2.1 antibody, was reduced only in direct proportion to the number of Lyb-2.1 cells present. The PFC response of Lyb-2.1/Lyb-2.2 heterozygous cells was not reduced by Lyb-2.1 antibody, presumably because generation of PFC is impeded only if most Lyb-2 sites are blocked. Further evidence that the molecule identified by Lyb-2 plays a critical role in the generation of antibody-forming cells (AFC) in response to T-dependent antigen comes from the finding that Lyb-2 antibody does not reduce the PFC response to the T-independent antigens trinitrophenylated (TNP) Brucella abortus and TNP-FicolI, although elimination of Lyb-2(+) cells from the starting population by Lyb-2 antibody and complement reduces the PFC response to T- dependent and T-independent antigens alike. The Rockefeller University Press 1981-01-01 /pmc/articles/PMC2186058/ /pubmed/6969779 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 Yakura, H Shen, F-W Kaemmer, M Boyse, EA Lyb-2 system of mouse B cells. Evidence for a role in the generation of antibody-forming cells |
title | Lyb-2 system of mouse B cells. Evidence for a role in the generation of antibody-forming cells |
title_full | Lyb-2 system of mouse B cells. Evidence for a role in the generation of antibody-forming cells |
title_fullStr | Lyb-2 system of mouse B cells. Evidence for a role in the generation of antibody-forming cells |
title_full_unstemmed | Lyb-2 system of mouse B cells. Evidence for a role in the generation of antibody-forming cells |
title_short | Lyb-2 system of mouse B cells. Evidence for a role in the generation of antibody-forming cells |
title_sort | lyb-2 system of mouse b cells. evidence for a role in the generation of antibody-forming cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186058/ https://www.ncbi.nlm.nih.gov/pubmed/6969779 |
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