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      B Cell Development in the Spleen Takes Place in Discrete Steps and Is Determined by the Quality of B Cell Receptor–Derived Signals

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          Abstract

          Only mature B lymphocytes can enter the lymphoid follicles of spleen and lymph nodes and thus efficiently participate in the immune response. Mature, long-lived B lymphocytes derive from short-lived precursors generated in the bone marrow. We show that selection into the mature pool is an active process and takes place in the spleen. Two populations of splenic B cells were identified as precursors for mature B cells. Transitional B cells of type 1 (T1) are recent immigrants from the bone marrow. They develop into the transitional B cells of type 2 (T2), which are cycling and found exclusively in the primary follicles of the spleen. Mature B cells can be generated from T1 or T2 B cells.

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          Most cited references59

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          Clonal selection and learning in the antibody system.

          K Rajewsky (1996)
          Each antibody-producing B cell makes antibodies of unique specificity, reflecting a series of ordered gene rearrangements which must be successfully performed if the cell is to survive. A second selection process occurs during immune responses in which a new antibody repertoire is generated through somatic hypermutation. Here only mutants binding antigen with high affinity survive to become memory cells. Cells expressing autoreactive receptors are counter-selected at both stages. This stringent positive and negative selection allows the generation and diversification of cells while rigorously controlling their specificity.
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            A putative chemokine receptor, BLR1, directs B cell migration to defined lymphoid organs and specific anatomic compartments of the spleen.

            We describe the phenotype of gene-targeted mice lacking the putative chemokine receptor BLR1. In normal mice, this receptor is expressed on mature B cells and a subpopulation of T helper cells. Blr1 mutant mice lack inguinal lymph nodes and possess no or only a few phenotypically abnormal Peyer's patches. The migration of lymphocytes into splenic follicles is severely impaired, resulting in morphologically altered primary lymphoid follicles. Furthermore, activated B cells fail to migrate from the T cell-rich zone into B cell follicles of the spleen, and despite high numbers of germinal center founder cells, no functional germinal centers develop in this organ. Our results identify the putative chemokine receptor BLR1 as the first G protein-coupled receptor involved in B cell migration and localization of these cells within specific anatomic compartments.
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              Lymphocyte homing and leukocyte rolling and migration are impaired in L-selectin-deficient mice.

              L-selectin, a cell adhesion molecule expressed by leukocytes, mediates the attachment of lymphocytes to high endothelial venules (HEV) of peripheral lymph nodes and mediates the earliest interactions between leukocytes and activated vascular endothelium. Mice possessing a mutant L-selectin gene that results in the complete loss of cell surface receptor expression were generated by gene targeting. Lymphocytes from these mice did not bind to peripheral lymph node HEV and these mice had a severe reduction in the number of lymphocytes localized to peripheral lymph nodes. Short-term homing experiments demonstrated that L-selectin was also involved in lymphocyte migration to mucosal lymph nodes, Peyer's patches, and spleen. Furthermore, significant defects in leukocyte rolling and neutrophil migration into the peritoneum in response to an inflammatory stimulus were observed. Thus, L-selectin plays an essential role in leukocyte homing to lymphoid tissues and sites of inflammation.
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                Author and article information

                Journal
                J Exp Med
                The Journal of Experimental Medicine
                The Rockefeller University Press
                0022-1007
                1540-9538
                1 July 1999
                : 190
                : 1
                : 75-90
                Affiliations
                [a ]From the Department of Molecular Immunology, Institute of Biology III, University of Freiburg, and the Max-Planck-Institute for Immunobiology, D-79108 Freiburg, Germany
                [b ]Department of Developmental Immunology, Max-Planck-Institute for Immunobiology, D-79108 Freiburg, Germany
                [c ]Wellesley Hospital Research Institute, Toronto, Ontario M4Y 1J3, Canada
                [d ]Department of Applied Cellular and Molecular Biology, Umeå University, S-901 87 Umeå, Sweden
                [e ]Basel Institute for Immunology, 4005 Basel, Switzerland
                Article
                98-2011
                10.1084/jem.190.1.75
                2195560
                10429672
                3eefc59f-e2ea-4000-b786-cdb1f79681ec
                © 1999 The Rockefeller University Press
                History
                : 16 November 1998
                : 22 April 1999
                : 5 May 1999
                Categories
                Original Article

                Medicine
                b cell development,transitional b cells,spleen,cd45,bruton's tyrosine kinase
                Medicine
                b cell development, transitional b cells, spleen, cd45, bruton's tyrosine kinase

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