B细胞缺陷型小鼠不会患上II型胶原诱导性关节炎（CIA）。
B cell-deficient mice do not develop type II collagen-induced arthritis (CIA).
作者信息
Svensson L, Jirholt J, Holmdahl R, Jansson L
机构信息
Section for Medical Inflammation Research, CMB, Lund University, Sweden.
出版信息
Clin Exp Immunol. 1998 Mar;111(3):521-6. doi: 10.1046/j.1365-2249.1998.00529.x.
Abstract
To investigate the role of B cells in the development of CIA, a model for rheumatoid arthritis, we investigated susceptibility to CIA in mice lacking B cells due to the deletion of the IgM heavy chain gene (muMT). The muMT deletion was backcrossed into two different CIA-susceptible strains, B10.Q and B10.RIII. Two different variants of the CIA model are inducible in these strains: in B10.Q with rat type II collagen (CII) and in B10.RIII with bovine CII. Homozygous deletion of the IgM gene led to the absence of B cells and dramatically reduced immunoglobulin levels compared with wild-type mice. The deletion of IgM totally abrogated development of CIA in both strains, although the anti-CII T cell response did not differ between the muMT and wild-type controls. We conclude that B cells play a crucial role in the development of CIA.
摘要
为了研究B细胞在类风湿性关节炎模型——胶原诱导性关节炎（CIA）发病过程中的作用，我们研究了因IgM重链基因（muMT）缺失而缺乏B细胞的小鼠对CIA的易感性。将muMT缺失基因回交到两种不同的CIA易感品系B10.Q和B10.RIII中。在这些品系中可诱导出两种不同的CIA模型变体：在B10.Q品系中用大鼠II型胶原（CII）诱导，在B10.RIII品系中用牛CII诱导。与野生型小鼠相比，IgM基因的纯合缺失导致B细胞缺失，并显著降低免疫球蛋白水平。尽管muMT小鼠与野生型对照之间的抗CII T细胞反应没有差异，但IgM的缺失完全消除了这两种品系中CIA的发病。我们得出结论，B细胞在CIA发病过程中起关键作用。
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