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B-Inducing Kinase1
*
First Department of Internal Medicine, Ehime University School of Medicine, Ehime, Japan; and
Division of Informative Cytology, Institute for Enzyme Research, University of Tokushima, Tokushima, Japan
Alymphoplasia (aly) mice, a natural strain with a
mutant NF-
B-inducing kinase (NIK) gene, manifest a unique phenotype;
they lack lymph nodes and Peyer’s patches, have a disturbed spleen
architecture, and exhibit defects in both Ab and cellular immune
responses. Although a stromal defect caused by impaired lymphotoxin-ß
receptor signaling accounts for their abnormal lymphoid organogenesis,
the exact mechanisms underlying the development of immunodeficiency in
aly mice are poorly understood. We therefore
investigated the contribution of hemopoietic cells with the
aly NIK mutation to the development of immunodeficiency.
Transfer of aly/aly bone marrow cells
into aly/+ mice resulted in poorly developed B cell
follicles and lack of support for the development of germinal centers
and isotype switching, indicating that the hemopoietic cells of
aly mice contain an autonomous defect. However,
follicular dendritic cell clusters were maintained in the spleens of
these bone marrow chimeras, suggesting that the lack of follicular
dendritic cell clusters in aly mice is probably due to
the stromal defect. The aly mice lacked marginal zone B
cells in their spleens, and aly/aly B
cells showed an impaired proliferative response after in vitro
stimulation. IL-2 production by activated T cells was also impaired. By
contrast, the dendritic cells of aly mice exhibited
grossly normal development and function. Supporting the concept of an
autonomous cell defect, Rel protein expression was altered in
aly/aly spleens. Thus, the
aly NIK mutation affects hemopoietic cell function in an
intrinsic fashion and, together with the stromal defect, may contribute
to the development of immunodeficiency in aly
mice.
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