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Disruption of the Bcl6 gene results in an impaired germinal center formation.

Fukuda T, Yoshida T, Okada S, Hatano M, Miki T, Ishibashi K, Okabe S, Koseki H, Hirosawa S, Taniguchi M, Miyasaka N, Tokuhisa T - J. Exp. Med. (1997)

Bottom Line: Lymphogenesis in primary lymphoid tissues of Bcl6(-/-)RM is normal, and Bcl6(-/-)RM produced control levels of primary IgG1 antibodies specific to T cell-dependent antigens.This defect was mainly due to the abnormalities of B cells.Therefore, Bcl6 is essential for the differentiation of GC B cells.

View Article: PubMed Central - PubMed

Affiliation: Division of Developmental Genetics, Center for Biomedical Science, Chiba University School of Medicine, Chiba, Japan.

ABSTRACT
The Bcl6 gene has been identified from the chromosomal translocation breakpoint in B cell lymphomas, and its products are expressed highly in germinal center (GC) B cells. To investigate the function of Bcl6 in lymphocytes, we have generated RAG1-deficient mice reconstituted with bone marrow cells from Bcl6-deficient mice (Bcl6(-/-)RM). Lymphogenesis in primary lymphoid tissues of Bcl6(-/-)RM is normal, and Bcl6(-/-)RM produced control levels of primary IgG1 antibodies specific to T cell-dependent antigens. However, GCs were not found in these mice. This defect was mainly due to the abnormalities of B cells. Therefore, Bcl6 is essential for the differentiation of GC B cells.

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Proliferation capacity of splenic B cells from Bcl6−/−RM.  Proliferative responses of splenic B cells from Bcl6+/+RM (shaded bars)  and Bcl6−/−RM (closed bars) to indicated stimuli. Results represent means  and variations (SD) from triplicate cultures. The data presented are representative of three independent experiments.
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Figure 8: Proliferation capacity of splenic B cells from Bcl6−/−RM. Proliferative responses of splenic B cells from Bcl6+/+RM (shaded bars) and Bcl6−/−RM (closed bars) to indicated stimuli. Results represent means and variations (SD) from triplicate cultures. The data presented are representative of three independent experiments.

Mentions: We then examined the capacity for proliferation of mature B cells from Bcl6−/−RM in vitro. Splenic B cells from Bcl6−/−RM were stimulated with LPS, LPS plus IL-4, anti-IgM Ab, CD40L, or anti-IgM plus CD40L. DNA synthesis of these stimulated cells was analyzed on day 2 after stimulation. Splenic B cells from Bcl6−/−RM proliferated well against these stimuli similar to those from Bcl6+/+RM (Fig. 8). Therefore, antigen-reactive B cells in Bcl6−/−RM may have a capacity to proliferate by antigen stimulations and signals from helper T cells in PALS.


Disruption of the Bcl6 gene results in an impaired germinal center formation.

Fukuda T, Yoshida T, Okada S, Hatano M, Miki T, Ishibashi K, Okabe S, Koseki H, Hirosawa S, Taniguchi M, Miyasaka N, Tokuhisa T - J. Exp. Med. (1997)

Proliferation capacity of splenic B cells from Bcl6−/−RM.  Proliferative responses of splenic B cells from Bcl6+/+RM (shaded bars)  and Bcl6−/−RM (closed bars) to indicated stimuli. Results represent means  and variations (SD) from triplicate cultures. The data presented are representative of three independent experiments.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2199007&req=5

Figure 8: Proliferation capacity of splenic B cells from Bcl6−/−RM. Proliferative responses of splenic B cells from Bcl6+/+RM (shaded bars) and Bcl6−/−RM (closed bars) to indicated stimuli. Results represent means and variations (SD) from triplicate cultures. The data presented are representative of three independent experiments.
Mentions: We then examined the capacity for proliferation of mature B cells from Bcl6−/−RM in vitro. Splenic B cells from Bcl6−/−RM were stimulated with LPS, LPS plus IL-4, anti-IgM Ab, CD40L, or anti-IgM plus CD40L. DNA synthesis of these stimulated cells was analyzed on day 2 after stimulation. Splenic B cells from Bcl6−/−RM proliferated well against these stimuli similar to those from Bcl6+/+RM (Fig. 8). Therefore, antigen-reactive B cells in Bcl6−/−RM may have a capacity to proliferate by antigen stimulations and signals from helper T cells in PALS.

Bottom Line: Lymphogenesis in primary lymphoid tissues of Bcl6(-/-)RM is normal, and Bcl6(-/-)RM produced control levels of primary IgG1 antibodies specific to T cell-dependent antigens.This defect was mainly due to the abnormalities of B cells.Therefore, Bcl6 is essential for the differentiation of GC B cells.

View Article: PubMed Central - PubMed

Affiliation: Division of Developmental Genetics, Center for Biomedical Science, Chiba University School of Medicine, Chiba, Japan.

ABSTRACT
The Bcl6 gene has been identified from the chromosomal translocation breakpoint in B cell lymphomas, and its products are expressed highly in germinal center (GC) B cells. To investigate the function of Bcl6 in lymphocytes, we have generated RAG1-deficient mice reconstituted with bone marrow cells from Bcl6-deficient mice (Bcl6(-/-)RM). Lymphogenesis in primary lymphoid tissues of Bcl6(-/-)RM is normal, and Bcl6(-/-)RM produced control levels of primary IgG1 antibodies specific to T cell-dependent antigens. However, GCs were not found in these mice. This defect was mainly due to the abnormalities of B cells. Therefore, Bcl6 is essential for the differentiation of GC B cells.

Show MeSH
Related in: MedlinePlus