Zhao Lintao, Liu Lina, Gao Jianbao, Yang Yang, Hu Chunyan, Guo Bo, Zhu Bo
Institution of Cancer, Xinqiao Hospital, Third Military Mediecal University, Chongqing 400037, China.
BMC Immunol. 2014 Sep 30;15:33. doi: 10.1186/s12865-014-0033-4.
Although a lot is known about how Fibroblastic Reticular Cells (FRCs) can regulate T lymphocytes (T cells), little is understood about whether or how T cells can regulate FRCs.
This study shows that the absence of T cells inhibited the secretion of ER-TR7 by splenic FRCs, induced the structural disorder of FRCs, down-regulated the expression of the chemokine ligands CCL21 and CCL19, and weakened the homing ability of T cells to the spleen of nude mice. Transfusion of T cells from BALB/c mice restored the structure and functions of FRCs and recovered them. The expression of lymphotoxin (LT)-B was significantly downregulated in the absence of T cells from nude mice and was recovered after the transfusion of T cells. After the occlusion of the LT-B receptor, the FRCs' structure and functions were not restored by transfusion of T cells.
These data reveal that the absence of T cells will subject spleen FRCs to structural and functional abnormality, and weaken the homing ability of T cells to the spleen. These changes are attributed to the T-cell- derived LT-B.
尽管人们对成纤维网状细胞（FRCs）如何调节T淋巴细胞（T细胞）了解很多，但对于T细胞是否能够以及如何调节FRCs却知之甚少。
本研究表明，T细胞缺失会抑制脾脏FRCs分泌ER-TR7，诱导FRCs结构紊乱，下调趋化因子配体CCL21和CCL19的表达，并削弱T细胞归巢至裸鼠脾脏的能力。输注来自BALB/c小鼠的T细胞可恢复FRCs的结构和功能。在裸鼠T细胞缺失时，淋巴毒素（LT）-B的表达显著下调，输注T细胞后恢复。阻断LT-B受体后，输注T细胞不能恢复FRCs的结构和功能。
这些数据表明，T细胞缺失会使脾脏FRCs出现结构和功能异常，并削弱T细胞归巢至脾脏的能力。这些变化归因于T细胞来源的LT-B。
