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J. Exp. Med.,
Volume 187, Number 2, January 19, 1998 185-196
B2 (p100/p52) Is Required for
Normal Splenic Microarchitecture and B Cell-mediated
Immune Responses
By
From the * Department of Oncology and the The nfkb2 gene is a member of the Rel/NF- Department of Experimental Pathology, Bristol-Myers
Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000; and the § Department
of Pathology, Uniformed Services, University of Health Sciences, Bethesda, Maryland 20814
B family of transcription factors. COOH-terminal deletions and rearrangements of this gene have been associated with the development of
human cutaneous T cell lymphomas, chronic lymphocytic leukemias, and multiple myelomas.
To further investigate the function of NF-B2, we have generated mutant mice carrying a germline mutation of the nfkb2 gene by homologous recombination. NF-B2-deficient mice
showed a marked reduction in the B cell compartment in spleen, bone marrow, and lymph
nodes. Moreover, spleen and lymph nodes of mutant mice presented an altered architecture,
characterized by diffuse, irregular B cell areas and the absence of discrete perifollicular marginal and mantle zones; the formation of secondary germinal centers in spleen was also impaired.
Proliferation of NF-B2-deficient B cells was moderately reduced in response to lipopolysaccharide, anti-IgD-dextran, and CD40, but maturation and immunoglobulin switching were
normal. However, nfkb2 (
/) animals presented a deficient immunological response to
T cell-dependent and -independent antigens. These findings indicate an important role of NF-B2 in the maintenance of the peripheral B cell population, humoral responses, and normal
spleen architecture.
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