Schrieber L, Steinberg A D, Rosenberg Y J, Csehi E E, Paull S A, Santoro T J
Rheumatol Int. 1986;6(5):215-9. doi: 10.1007/BF00541370.
The patterns of migration of lymphoid cells from autoimmune-prone MRL-lpr/lpr, C57BL/6-lpr/lpr, MRL-+/+, and NZB mice were compared to those from sex and age-matched, normal CBA, C57BL/6, and BALB/C mice. Chromium-51-labelled spleen and lymph node cells from all autoimmune mice tested homed preferentially to the spleen relative to lymph node of the recipient strain. The data indicate that defects in lymphocyte trafficking are widespread in murine lupus and suggest a role for abnormal lymphocyte migration in the pathogenesis of this disease.
将自身免疫易感的MRL-lpr/lpr、C57BL/6-lpr/lpr、MRL-+/+和NZB小鼠的淋巴细胞迁移模式与性别和年龄匹配的正常CBA、C57BL/6和BALB/C小鼠的淋巴细胞迁移模式进行了比较。相对于受体品系的淋巴结,所有受试自身免疫小鼠经铬-51标记的脾细胞和淋巴结细胞优先归巢至脾。数据表明,淋巴细胞运输缺陷在小鼠狼疮中广泛存在,并提示异常淋巴细胞迁移在该疾病发病机制中发挥作用。