EFFECT OF XID ON ANTI-DNA B-CELL PRECURSORS
EFFECT OF XID ON ANTI-DNA B-CELL PRECURSORS
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DOI：
10.1016/0008-8749(83)90287-3
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发表时间：
1983-01-01
影响因子：
4.3
通讯作者：
STEINBERG, AD
中科院分区：
文献类型：
--
作者：
PISETSKY, DS;CASTER, SA;STEINBERG, AD
通过对非xid和同源xid自身免疫小鼠和正常小鼠中产生抗DNA的B细胞的前体频率分析，研究了xid基因对小鼠自身免疫的影响。抗体反应在体外诱导脂多糖在有限稀释条件下与IgM抗DNA和抗三硝基苯基（TNP）确定为模型的自身抗体和非自身抗体，分别。所有小鼠均表现出抗DNA前体的高频率，而自身免疫（NZB和MRL-lpr/lpr）和非自身免疫（CBA/J和DBA/2）菌株之间无差异。在这些菌株中，xid基因的存在与抗DNA的显著减少相关。对于NZBxid小鼠，这种抗DNA前体的损失远大于抗TNP前体的损失，其频率与NZB小鼠相似。相对于非xid小鼠，携带xid的CBA/N、DBA/2xid和MLxid小鼠显示出抗DNA和抗TNP前体的显著降低。NZBxid小鼠的完整抗TNP应答可能是NZB品系免疫异常的另一种表现，表明它们的B细胞群在活化条件下不同于其他小鼠。由于NZBxid脾脏具有抗DNA应答的优先减少，这表明在NZB小鼠中，抗DNA抗体的前体主要分布在受xid影响的B细胞亚群中，解释了其自身抗体产生的消除。在非xid小鼠中，前体细胞的数量相等，表明从前体细胞到产生自身抗体的B细胞的变化存在额外的调节异常。
The influence of the xid gene on murine autoimmunity was investigated by precursor frequency analysis of anti-DNA-producing B cells in non-xid and congenic xid autoimmune and normal mice. Antibody responses were induced in vitro by lipopolysaccharides under limiting-dilution conditions with IgM anti-DNA and antitrinitrophenyl (TNP) determined as models of an autoantibody and nonautoantibody, respectively. All mice demonstrated high frequencies of precursors for anti-DNA without differences between the autoimmune (NZB and MRL-lpr/lpr) and nonautoimmune (CBA/J and DBA/2) strains. In these strains, the presence of the xid gene was associated with a marked reduction of anti-DNA. For NZBxid mice, this loss of anti-DNA precursors was much greater than that for anti-TNP precursors, whose frequency was similar to that of NZB mice. xid-Bearing CBA/N, DBA/2xid and MLxid mice showed marked reductions in both anti-DNA and anti-TNP precursors relative to non-xid mice. The intact anti-TNP response of NZBxid mice may be an additional manifestation of immune abnormalities of the NZB strain and suggests that their B-cell populations differ from those of other mice in the conditions for activation. Since NZBxid spleens had a preferential reduction of anti-DNA responses, which suggests that in NZB mice precursors for anti-DNA antibodies are predominantly distributed in the B-cell subset affected by xid, explaining the abrogation of their autoantibody production. The equivalent number of precursors in non-xid mice indicates that additional regulatory abnormalities underlie the change from precursor to autoantibody-producing B cell.