Nek2 Is a Novel Regulator of B Cell Development and Immunological Response
Nek2 Is a Novel Regulator of B Cell Development and Immunological Response
The serine/threonine kinase Nek2 is commonly found upregulated in a wide variety of neoplasms including diffuse large B cell lymphoma and multiple myeloma. High expression of Nek2 is implicated in the induction of chromosomal instability, promotion of cell proliferation, and drug resistance in tumor cells as well as a marker for poor clinical outcomes. Despite its well recorded involvement in chromosomal instability and neoplastic growth, little is known about the involvement of Nek2 in B cell development. Here we report the development of a transgenic mouse line with conditional expression of Nek2 in the B cell lineage and the effects it has on the development of B cells. Interestingly, we found that the overexpression of Nek2 does not induce spontaneous tumor formation within the transgenic mice up to 24 months after induction. Instead, overexpression of Nek2 in the B cell lineage affects the development of B cells by increasing the proportion of immature B cells in the bone marrow and decreasing B-1 B cells in peritoneal cavity. Furthermore, Nek2 transgenic mice develop spontaneous germinal centers and exhibit an enhanced T cell dependent immune response. Altogether, our data demonstrates a novel role for Nek2 in regulating B cell development and the immune response.
- University of Iowa United States
- UNIVERSITY OF IOWA
- UNIVERSITY OF UTAH
- University of Utah United States
- Roy J. and Lucille A. Carver College of Medicine United States
B-Lymphocytes, Lymphoma, B-Cell, T-Lymphocytes, Mice, Transgenic, Protein Serine-Threonine Kinases, Mice, Cell Line, Tumor, Animals, Humans, NIMA-Related Kinases, Cell Lineage, Multiple Myeloma, Research Article, Cell Proliferation
B-Lymphocytes, Lymphoma, B-Cell, T-Lymphocytes, Mice, Transgenic, Protein Serine-Threonine Kinases, Mice, Cell Line, Tumor, Animals, Humans, NIMA-Related Kinases, Cell Lineage, Multiple Myeloma, Research Article, Cell Proliferation
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