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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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B cells are responsible for the defect of GC formation in Bcl6−/− RM. Spleen sections from the DNP–OVA  immunized RAG1−/− reconstituted with B cells from Bcl6+/+  RM and T cells from Bcl6−/−  RM (A), or with B cells from  Bcl6−/−RM and T cells from  Bcl6+/+RM (B) were stained  with PNA (brown). Hematoxylin counterstain.
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Figure 6: B cells are responsible for the defect of GC formation in Bcl6−/− RM. Spleen sections from the DNP–OVA immunized RAG1−/− reconstituted with B cells from Bcl6+/+ RM and T cells from Bcl6−/− RM (A), or with B cells from Bcl6−/−RM and T cells from Bcl6+/+RM (B) were stained with PNA (brown). Hematoxylin counterstain.

Mentions: Functions of T cells in GCs are essential for GC formation of B cells (38, 39) and BCL6 is detected in a small fraction of CD4+ T cells in GCs (7). To determine whether defects in GC formation in Bcl6−/−RM are due to defects in B or T cells or both, splenic T and B cells were isolated from Bcl6−/−RM and Bcl6+/+RM and then co-transferred into RAG1−/− 1 d before immunization with DNP–OVA. GC formation in the spleen was histologically analyzed 2 wk later. GC formation was detected in spleens from mice reconstituted with B cells from Bcl6+/+RM and T cells from Bcl6−/−RM (Fig. 6 A). In contrast, co-transfer of B cells from Bcl6−/−RM and T cells from Bcl6+/+RM did not restore GC formation (Fig. 6 B), indicating that Bcl6 expression in B but not in T cells is essential for the GC formation.


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)

B cells are responsible for the defect of GC formation in Bcl6−/− RM. Spleen sections from the DNP–OVA  immunized RAG1−/− reconstituted with B cells from Bcl6+/+  RM and T cells from Bcl6−/−  RM (A), or with B cells from  Bcl6−/−RM and T cells from  Bcl6+/+RM (B) were stained  with PNA (brown). Hematoxylin counterstain.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 6: B cells are responsible for the defect of GC formation in Bcl6−/− RM. Spleen sections from the DNP–OVA immunized RAG1−/− reconstituted with B cells from Bcl6+/+ RM and T cells from Bcl6−/− RM (A), or with B cells from Bcl6−/−RM and T cells from Bcl6+/+RM (B) were stained with PNA (brown). Hematoxylin counterstain.
Mentions: Functions of T cells in GCs are essential for GC formation of B cells (38, 39) and BCL6 is detected in a small fraction of CD4+ T cells in GCs (7). To determine whether defects in GC formation in Bcl6−/−RM are due to defects in B or T cells or both, splenic T and B cells were isolated from Bcl6−/−RM and Bcl6+/+RM and then co-transferred into RAG1−/− 1 d before immunization with DNP–OVA. GC formation in the spleen was histologically analyzed 2 wk later. GC formation was detected in spleens from mice reconstituted with B cells from Bcl6+/+RM and T cells from Bcl6−/−RM (Fig. 6 A). In contrast, co-transfer of B cells from Bcl6−/−RM and T cells from Bcl6+/+RM did not restore GC formation (Fig. 6 B), indicating that Bcl6 expression in B but not in T cells is essential for the GC formation.

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