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-Deficient Mice and Alymphoplasia (aly) Mice Defined by the Chimeric Analysis1
*
First Department of Internal Medicine, School of Medicine, Ehime University, Ehime, Japan;
Division of Informative Cytology, Institute for Enzyme Research, University of Tokushima, Tokushima, Japan;
Department of Immunology and Inflammation, Biogen Inc., Cambridge, MA 02142;
Reproductive Engineering Section, Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan; and
¶
Genome Information Research Center, Osaka University, Osaka, Japan
Both lymphotoxin-
(LT)-deficient mice and alymphoplasia
(aly) mice, a natural mutant strain, manifest a quite
similar phenotype: lack of lymph nodes (LN) and Peyer’s patches (PP),
with disturbed spleen architecture. The mechanisms underlying the
defective lymphoid organogenesis in these mice were investigated by
generating aggregation chimeras; ex vivo fused morulae were implanted
into pseudo-pregnant host females and allowed to develop to term.
Chimeric mice between LT-deficient mice and wild-type mice restored
LN and PP almost completely, suggesting that LT expressed by
circulating bone marrow-derived cells is essential for lymphoid
organogenesis as well as for organization of spleen architecture. By
contrast, chimeric mice between aly mice and wild-type
mice showed only limited restoration of LN and PP. This suggests that
the putative aly gene product does not act as a
circulating ligand for lymphoid organogenesis, like LT. Rather,
abnormal development of lymphoid organs in aly mice
seems most likely due to the defective development of the incipient
stromal cells of the LN and PP. Supporting this hypothesis,
up-regulation of VCAM-1 on aly mouse embryonic
fibroblasts by signals through LT
R, which is exclusively expressed
by nonlymphoid cells, was disturbed. These studies demonstrate that
LT and the putative aly gene product together control
lymphoid organogenesis with a close mechanistic relationship in their
biochemical pathways through governing the distinct cellular
compartments, the former acting as a circulating ligand and the latter
as a LTR-signaling molecule expressed by the stroma of the lymphoid
organs.
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