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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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GC formation is impaired in spleen from Bcl6−/−RM. Splenocytes from Bcl6+/+RM (A) and Bcl6−/−RM (B) immunized with DNP–OVA  on day 14 after immunization were stained with PNA and anti-B220 Ab. The numbers in the figures indicate percentages of PNAhigh B220+ cells relative  to total B220+ cells. Splenic sections from the immunized Bcl6+/+RM (C and E) and Bcl6−/−RM (D and F) were stained with PNA (C and D) or anti-B220 Ab (E and F) (brown). Hematoxylin counterstain. G, germinal center; T, T cell–rich PALS; M, marginal zone; F, primary follicle.
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Figure 4: GC formation is impaired in spleen from Bcl6−/−RM. Splenocytes from Bcl6+/+RM (A) and Bcl6−/−RM (B) immunized with DNP–OVA on day 14 after immunization were stained with PNA and anti-B220 Ab. The numbers in the figures indicate percentages of PNAhigh B220+ cells relative to total B220+ cells. Splenic sections from the immunized Bcl6+/+RM (C and E) and Bcl6−/−RM (D and F) were stained with PNA (C and D) or anti-B220 Ab (E and F) (brown). Hematoxylin counterstain. G, germinal center; T, T cell–rich PALS; M, marginal zone; F, primary follicle.

Mentions: GC formation was histologically analyzed in spleens from mice immunized with DNP–OVA on day 14 after immunization. PNA-binding GC B cells were clearly identified in all of the Bcl6+/+RM analyzed (n = 8, Fig. 4, A and C). In contrast, none of the Bcl6−/−RM spleens (n = 8) showed PNA-binding B cells in follicles (Fig. 4, B and D), although primary B cell follicles, marginal zones, and PALS were histologically identified (Fig. 4 F).


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)

GC formation is impaired in spleen from Bcl6−/−RM. Splenocytes from Bcl6+/+RM (A) and Bcl6−/−RM (B) immunized with DNP–OVA  on day 14 after immunization were stained with PNA and anti-B220 Ab. The numbers in the figures indicate percentages of PNAhigh B220+ cells relative  to total B220+ cells. Splenic sections from the immunized Bcl6+/+RM (C and E) and Bcl6−/−RM (D and F) were stained with PNA (C and D) or anti-B220 Ab (E and F) (brown). Hematoxylin counterstain. G, germinal center; T, T cell–rich PALS; M, marginal zone; F, primary follicle.
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Related In: Results  -  Collection

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Figure 4: GC formation is impaired in spleen from Bcl6−/−RM. Splenocytes from Bcl6+/+RM (A) and Bcl6−/−RM (B) immunized with DNP–OVA on day 14 after immunization were stained with PNA and anti-B220 Ab. The numbers in the figures indicate percentages of PNAhigh B220+ cells relative to total B220+ cells. Splenic sections from the immunized Bcl6+/+RM (C and E) and Bcl6−/−RM (D and F) were stained with PNA (C and D) or anti-B220 Ab (E and F) (brown). Hematoxylin counterstain. G, germinal center; T, T cell–rich PALS; M, marginal zone; F, primary follicle.
Mentions: GC formation was histologically analyzed in spleens from mice immunized with DNP–OVA on day 14 after immunization. PNA-binding GC B cells were clearly identified in all of the Bcl6+/+RM analyzed (n = 8, Fig. 4, A and C). In contrast, none of the Bcl6−/−RM spleens (n = 8) showed PNA-binding B cells in follicles (Fig. 4, B and D), although primary B cell follicles, marginal zones, and PALS were histologically identified (Fig. 4 F).

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