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Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice

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Standard

Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice. / Andersen, Sonja; Ericsson, Madelene; Dai, Hong Yan; Pena Diaz, Javier; Slupphaug, Geir; Nilsen, Hilde; Aarset, Harald; Krokan, Hans E.

I: DNA Repair, Bind 4, Nr. 12, 08.12.2005, s. 1432-41.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Andersen, S, Ericsson, M, Dai, HY, Pena Diaz, J, Slupphaug, G, Nilsen, H, Aarset, H & Krokan, HE 2005, 'Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice', DNA Repair, bind 4, nr. 12, s. 1432-41. https://doi.org/10.1016/j.dnarep.2005.08.004

APA

Andersen, S., Ericsson, M., Dai, H. Y., Pena Diaz, J., Slupphaug, G., Nilsen, H., ... Krokan, H. E. (2005). Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice. DNA Repair, 4(12), 1432-41. https://doi.org/10.1016/j.dnarep.2005.08.004

Vancouver

Andersen S, Ericsson M, Dai HY, Pena Diaz J, Slupphaug G, Nilsen H o.a. Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice. DNA Repair. 2005 dec 8;4(12):1432-41. https://doi.org/10.1016/j.dnarep.2005.08.004

Author

Andersen, Sonja ; Ericsson, Madelene ; Dai, Hong Yan ; Pena Diaz, Javier ; Slupphaug, Geir ; Nilsen, Hilde ; Aarset, Harald ; Krokan, Hans E. / Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice. I: DNA Repair. 2005 ; Bind 4, Nr. 12. s. 1432-41.

Bibtex

@article{f7214ab65b2f4f8e905825efd3426b99,
title = "Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice",
abstract = "Ung-deficient mice have reduced class switch recombination, skewed somatic hypermutation, lymphatic hyperplasia and a 22-fold increased risk of developing B-cell lymphomas. We find that lymphomas are of follicular (FL) and diffuse large B-cell type (DLBCL). All FLs and 75{\%} of the DLBCLs were monoclonal while 25{\%} were biclonal. Monoclonality was also observed in hyperplasia, and could represent an early stage of lymphoma development. Lymphoid hyperplasia occurs very early in otherwise healthy Ung-deficient mice, observed as a significant increase of splenic B-cells. Furthermore, loss of Ung also causes a significant reduction of T-helper cells, and 50{\%} of the young Ung(-/-) mice investigated have no detectable NK/NKT-cell population in their spleen. The immunological imbalance is confirmed in experiments with spleen cells where the production of the cytokines interferon gamma, interleukin 6 and interleukin 2 is clearly different in wild type and in Ung-deficient mice. This suggests that Ung-proteins, directly or indirectly, have important functions in the immune system, not only in the process of antibody maturation, but also for production and functions of immunologically important cell types. The immunological imbalances shown here in the Ung-deficient mice may be central in the development of lymphomas in a background of generalised lymphoid hyperplasia.",
keywords = "Animals, B-Lymphocytes, Concanavalin A, Cytokines, DNA, Flow Cytometry, Gene Expression Profiling, Genotype, Hyperplasia, Lectins, Leukocytes, Lipopolysaccharides, Lymphoma, B-Cell, Mice, Spleen, T-Lymphocytes, Tetradecanoylphorbol Acetate, Uracil-DNA Glycosidase",
author = "Sonja Andersen and Madelene Ericsson and Dai, {Hong Yan} and {Pena Diaz}, Javier and Geir Slupphaug and Hilde Nilsen and Harald Aarset and Krokan, {Hans E}",
year = "2005",
month = "12",
day = "8",
doi = "10.1016/j.dnarep.2005.08.004",
language = "English",
volume = "4",
pages = "1432--41",
journal = "D N A Repair",
issn = "1568-7864",
publisher = "Elsevier",
number = "12",

}

RIS

TY - JOUR

T1 - Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice

AU - Andersen, Sonja

AU - Ericsson, Madelene

AU - Dai, Hong Yan

AU - Pena Diaz, Javier

AU - Slupphaug, Geir

AU - Nilsen, Hilde

AU - Aarset, Harald

AU - Krokan, Hans E

PY - 2005/12/8

Y1 - 2005/12/8

N2 - Ung-deficient mice have reduced class switch recombination, skewed somatic hypermutation, lymphatic hyperplasia and a 22-fold increased risk of developing B-cell lymphomas. We find that lymphomas are of follicular (FL) and diffuse large B-cell type (DLBCL). All FLs and 75% of the DLBCLs were monoclonal while 25% were biclonal. Monoclonality was also observed in hyperplasia, and could represent an early stage of lymphoma development. Lymphoid hyperplasia occurs very early in otherwise healthy Ung-deficient mice, observed as a significant increase of splenic B-cells. Furthermore, loss of Ung also causes a significant reduction of T-helper cells, and 50% of the young Ung(-/-) mice investigated have no detectable NK/NKT-cell population in their spleen. The immunological imbalance is confirmed in experiments with spleen cells where the production of the cytokines interferon gamma, interleukin 6 and interleukin 2 is clearly different in wild type and in Ung-deficient mice. This suggests that Ung-proteins, directly or indirectly, have important functions in the immune system, not only in the process of antibody maturation, but also for production and functions of immunologically important cell types. The immunological imbalances shown here in the Ung-deficient mice may be central in the development of lymphomas in a background of generalised lymphoid hyperplasia.

AB - Ung-deficient mice have reduced class switch recombination, skewed somatic hypermutation, lymphatic hyperplasia and a 22-fold increased risk of developing B-cell lymphomas. We find that lymphomas are of follicular (FL) and diffuse large B-cell type (DLBCL). All FLs and 75% of the DLBCLs were monoclonal while 25% were biclonal. Monoclonality was also observed in hyperplasia, and could represent an early stage of lymphoma development. Lymphoid hyperplasia occurs very early in otherwise healthy Ung-deficient mice, observed as a significant increase of splenic B-cells. Furthermore, loss of Ung also causes a significant reduction of T-helper cells, and 50% of the young Ung(-/-) mice investigated have no detectable NK/NKT-cell population in their spleen. The immunological imbalance is confirmed in experiments with spleen cells where the production of the cytokines interferon gamma, interleukin 6 and interleukin 2 is clearly different in wild type and in Ung-deficient mice. This suggests that Ung-proteins, directly or indirectly, have important functions in the immune system, not only in the process of antibody maturation, but also for production and functions of immunologically important cell types. The immunological imbalances shown here in the Ung-deficient mice may be central in the development of lymphomas in a background of generalised lymphoid hyperplasia.

KW - Animals

KW - B-Lymphocytes

KW - Concanavalin A

KW - Cytokines

KW - DNA

KW - Flow Cytometry

KW - Gene Expression Profiling

KW - Genotype

KW - Hyperplasia

KW - Lectins

KW - Leukocytes

KW - Lipopolysaccharides

KW - Lymphoma, B-Cell

KW - Mice

KW - Spleen

KW - T-Lymphocytes

KW - Tetradecanoylphorbol Acetate

KW - Uracil-DNA Glycosidase

U2 - 10.1016/j.dnarep.2005.08.004

DO - 10.1016/j.dnarep.2005.08.004

M3 - Journal article

C2 - 16174566

VL - 4

SP - 1432

EP - 1441

JO - D N A Repair

JF - D N A Repair

SN - 1568-7864

IS - 12

ER -

ID: 138821403