ID 21957
著者
松本, 満 Division of Informative Cytology, Institute for Enzyme Research, University of Tokushima 徳島大学 教育研究者総覧 KAKEN研究者をさがす
キーワード
lymphotoxin
TNF
lymph node
spleen
knockout mice
資料タイプ
学術雑誌論文
抄録
The molecular basis of lymphoid organogenesis has recently been elucidated using gene-targeted mice. Mice deficient in lymphotoxin-α (LTα) lack lymph nodes and Peyer's patches. The action of LTα in lymphoid organogenesis is mediated mostly by the membrane form of LT by a mechanism independent of TNF receptor I (TNFR-I) or II (TNFR-II). Additionally, follicular dendritic cell (FDC) clusters or germinal centers fail to develop in the spleen of LTα-deficient mice. Mice deficient in either TNFR-I or LTβR also fail to develop splenic FDC clusters and germinal centers, indicating that signaling through both TNFR-I and LTβR is required for the development of these structures. The mechanisms underlying the defective lymphoid organogenesis in LTα-deficient mice, together with a natural mutant strain, alymphoplasia (aly) mice, which manifest a quite similar phenotype to LTα-deficient mice, were investigated by generating aggregation chimeras. These studies demonstrate that LTα and the aly gene product together control lymphoid organogenesis with a close mechanistic relationship in their biochemical pathways through governing distinct cellular compartments;the former acting as a circulating ligand and the latter as a LTβR-signaling molecule expressed by the stroma of the lymphoid organs.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
46
3-4
開始ページ
141
終了ページ
150
並び順
141
発行日
1999
備考
EDB ID
フルテキストファイル
言語
eng
部局
先端酵素学研究所