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Articles |
B2 (p100/p52) Is Required for Normal Splenic Microarchitecture and B Cell–mediated Immune Responses
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
The nfkb2 gene is a member of the Rel/NF-
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.
1 Abbreviations used in this paper: EMSA, electrophoretic mobility shift assays; ES, embryonic stem; FDC, follicular dendritic cell; GC, germinal center; PNA, peanut agglutinin; SRBC, sheep red blood cell.
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