Expression pattern changes and function of RANKL during mouse lymph node microarchitecture development
Expression pattern changes and function of RANKL during mouse lymph node microarchitecture development
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DOI：
10.1093/intimm/dxs002
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发表时间：
2012-06-01
影响因子：
4.4
通讯作者：
Yoshida, Hisahiro
中科院分区：
文献类型：
--
作者：
Sugiyama, Machiko;Nakato, Gaku;Yoshida, Hisahiro
核因子κ B受体激活因子配体（RANKL）的表达在小鼠胎儿外周淋巴器官的发育过程中进行了检查。在从淋巴组织诱导（LTi）细胞的淋巴结（LN）的原基，但不是在派尔集合淋巴结原基的淋巴组织形成（LTo）细胞的过渡过程中检测到的表达模式的转变。为了了解这些变化对胎儿RANKL表达的功能影响，通过阻断抗体阻断RANKL功能。在13.5至16.5 dpc之间向妊娠小鼠施用过量的抗RANKL抗体，发现其完全阻断LN原基的发育，表明在此期间RANKL功能对LN发育至关重要。此外，在13.5 dpc时将少量抗RANKL抗体直接注射到羊膜腔中，导致出生后B细胞卵泡形成紊乱和高内皮微静脉分化。这些结果表明，在LN发展的早期阶段，RANKL在LTi细胞上的表达对于LN微结构的发展至关重要。
Receptor activator of nuclear factor kappa-B ligand (RANKL) expression was examined during the development of mouse fetal peripheral lymphoid organs. A shift in the expression pattern was detected during the transition from lymphoid tissue inducer (LTi) cells to lymphoid tissue organizer (LTo) cells in the lymph node (LN) anlagen but not in the Peyer's patch anlagen. In order to understand the functional impact of these changes in the fetal expression of RANKL, the RANKL function was blocked by a blocking antibody. Excess anti-RANKL antibody was administered to pregnant mice between 13.5 and 16.5 dpc and was found to completely block LN anlagen development, suggesting that RANKL function during this period is critical for LN development. In addition, small amounts of anti-RANKL antibodies were injected directly into the amniotic space at 13.5 dpc, resulting in perturbed B-cell follicle formation and high endothelial venule differentiation after birth. These results suggest that RANKL expression on LTi cells during the early phase of LN development is critical for the development LN microarchitecture.