Serum autoantibodies in pristane induced lupus are regulated by neutrophil gelatinase associated lipocalin.
Serum autoantibodies in pristane induced lupus are regulated by neutrophil gelatinase associated lipocalin.
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DOI：
10.1016/j.clim.2014.06.007
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发表时间：
2014-09
期刊：
影响因子：
--
通讯作者：
Putterman C
中科院分区：
文献类型：
--
作者：
Pawar RD;Goilav B;Xia Y;Zhuang H;Herlitz L;Reeves WH;Putterman C
在系统性自身免疫中，自身抗体的出现可能是多个检查点耐受能力下降的结果。遗传、激素和免疫因素可与环境影响相结合，加速疾病的发生，加重疾病结局。在这里，我们描述了一种与中性粒细胞明胶酶相关脂钙蛋白（NGAL）在调节普里坦诱导狼疮自身抗体水平中的调节作用有关的新机制。单次腹腔注射普利斯坦后，血清和脾脏均诱导NGAL表达。此外，NGAL缺陷小鼠更容易诱导pristane刺激的自身免疫，脾脏中自身抗体分泌细胞数量增加，激活诱导胞苷脱氨酶（AID）和其他炎症介质的表达增加。相反，NGAL缺乏小鼠的肾脏损伤较轻，表明NGAL在自身抗体介导的肾脏疾病中是有害的。这些研究表明，NGAL在狼疮的不同组织中起着不同的作用，并提示NGAL在适应性免疫中的作用以前未被认识到。
The onset of autoantibodies in systemic autoimmunity can be the result of a breakdown in tolerance at multiple checkpoints. Genetic, hormonal, and immunological factors can combine with environmental influences to accelerate the onset of disease and aggravate disease outcome. Here, we describe a novel mechanism relating to the regulatory role of Neutrophil Gelatinase Associated Lipocalin (NGAL) in modulating the levels of autoantibodies in pristane induced lupus. Following a single injection of pristane intraperitoneally, NGAL expression was induced in both the serum and spleen. Furthermore, NGAL deficient mice were more susceptible to the induction of pristane stimulated autoimmunity, and displayed higher numbers of autoantibody secreting cells and increased expression of activation induced cytidine deaminase (AID) and other inflammatory mediators in the spleen. In contrast, kidney damage was milder in NGAL deficient mice, indicating that NGAL was detrimental in autoantibody mediated kidney disease. These studies indicate that NGAL plays differential roles in different tissues in the context of lupus, and suggest a previously unrecognized role for NGAL in adaptive immunity.
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影响因子：
11.2
作者：
Chakraborty, Subhankar;Kaur, Sukhwinder;Guha, Sushovan;Batra, Surinder K.
通讯作者：
Batra, Surinder K.
影响因子：
3.3
作者：
Gao, Hua-Xin;Sanders, Elena;Putterman, Chaim
通讯作者：
Putterman, Chaim
影响因子：
4.4
作者：
Deocharan, B;Qing, XP;Putterman, C
通讯作者：
Putterman, C
影响因子：
4.4
作者：
Kikawada, E;Lenda, DM;Kelley, VR
通讯作者：
Kelley, VR
DOI：
10.1073/pnas.0510847103
发表时间：
2006-02-07
影响因子：
11.1
作者：
Berger, T;Togawa, A;Mak, TW
通讯作者：
Mak, TW