Passive transfer autoimmunity in a mouse model of complex regional pain syndrome.
Passive transfer autoimmunity in a mouse model of complex regional pain syndrome.
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DOI：
10.1097/j.pain.0000000000001046
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发表时间：
2017-12
期刊：
影响因子：
7.4
通讯作者：
Kingery WS
中科院分区：
文献类型：
--
作者：
Guo TZ;Shi X;Li WW;Wei T;Clark JD;Kingery WS
复杂区域疼痛综合征(CRPS)被认为是一种创伤后自身免疫性疾病，我们先前在小鼠胫骨骨折CRPS模型中观察到需要B细胞才能充分表达CRPS样变。目前的研究使用小鼠模型来评估缺乏B细胞和抗体的野生型(WT)和木乃伊骨折小鼠骨折后CRPS样变化的进展。本实验还评价了WT骨折小鼠血清抗体对木乃伊骨折小鼠的致痛作用。骨折后疼痛行为从骨折后3周开始依赖于先天和自身免疫性炎症机制，到骨折后12周完全由抗体调节，到骨折后21周自然消退。此外，WT骨折小鼠的血清IgM抗体注射到木乃伊骨折小鼠后，对骨折肢体具有促伤害性作用。IGM抗体水平在骨折肢体后爪皮肤、坐骨神经和相应的腰髓中逐渐升高，在骨折后12-18周达到峰值，然后下降。免疫组织化学染色显示骨折后IgM抗体与骨折肢体后爪真皮细胞核中的抗原结合。我们推测，骨折可以诱导骨折肢体皮肤、坐骨神经和脊髓中新抗原的表达，从而触发B细胞分泌结合这些抗原的IgM抗体，并启动伤害性抗体反应。在小鼠骨折模型中，自身免疫在伤害性和血管变化的进展中起着关键作用，并可能参与CRPS疾病的进程。
It has been proposed that Complex Regional Pain Syndrome (CRPS) is a post-traumatic autoimmune disease and we previously observed that B cells are required for the full expression of CRPS-like changes a mouse tibia fracture CRPS model. The current study used the mouse model to evaluate the progression of post-fracture CRPS-like changes in wildtype (WT) and muMT fracture mice lacking B cells and antibodies. The pronociceptive effects of injecting WT fracture mouse serum antibodies into muMT fracture mice were also evaluated. Post-fracture pain behaviors transitioned from being initially dependent on both innate and autoimmune inflammatory mechanisms at 3 weeks post-fracture to being entirely mediated by antibody responses at 12 weeks post-fracture and spontaneously resolving by 21 weeks post-fracture. Furthermore, serum IgM antibodies from WT fracture mice had pronociceptive effects in the fracture limb when injected into muMT fracture mice. IgM antibody levels gradually increased in the fracture limb hindpaw skin, sciatic nerve, and corresponding lumbar cord, peaking at 12–18 weeks post-fracture and then declining. Immunohistochemistry localized post-fracture IgM antibody binding to antigens in the fracture limb hindpaw dermal cell nuclei. We postulate that fracture induces expression of neoantigens in fracture limb skin, sciatic nerve, and cord, which trigger B cells to secret IgM antibodies that bind those antigens and initiate a pronociceptive antibody response. Autoimmunity plays a key role in the progression of nociceptive and vascular changes in the mouse fracture model and potentially contributors to the CRPS disease process.
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小鼠复杂区域疼痛综合征的急性和慢性阶段伴随着脊髓的不同转录变化。
影响因子：
3.3
作者：
Gallagher JJ;Tajerian M;Guo T;Shi X;Li W;Zheng M;Peltz G;Kingery WS;Clark JD
通讯作者：
Clark JD
影响因子：
4.6
作者：
Huygen, FJPM;de Bruijn, AGJ;Zijlstra, FJ
通讯作者：
Zijlstra, FJ
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影响因子：
7.4
作者：
Beerthuizen, Annemerle;Stronks, Dirk L.;Huygen, Frank J. P. M.
通讯作者：
Huygen, Frank J. P. M.
影响因子：
4
作者：
Birklein, Frank;Drummond, Peter D.;Li, Wenwu;Schlereth, Tanja;Albrecht, Nahid;Finch, Philip M.;Dawson, Linda F.;Clark, J. David;Kingery, Wade S.
通讯作者：
Kingery, Wade S.
影响因子：
7.4
作者：
Jang JH;Clark DJ;Li X;Yorek MS;Usachev YM;Brennan TJ
通讯作者：
Brennan TJ