Laboratory for Neuropathology, Department of Neurology, Ghent University Hospital, Ghent, Belgium.
Neuromuscul Disord. 2012 Aug;22(8):712-9. doi: 10.1016/j.nmd.2012.04.012. Epub 2012 May 30.
Lymphotoxin beta (LTβ) regulates some inflammatory mechanisms that could be operative in idiopathic inflammatory myopathies (IM). We studied LTβ and LTβR in inflammatory myopathies, normal and disease controls with immunohistochemistry, Western blotting and in situ hybridisation. LTβ occurs in myonuclei of normal controls, implying its role in normal muscle physiology. LTβ is strongly upregulated in regenerating muscle fibres in all myopathies, but not in denervated myofibres. Normal-appearing myofibres in inflammatory myopathies and muscular dystrophies express LTβ possibly reflecting early myofibre damage, representing a hitherto undescribed pathologic hallmark. Furthermore, we visualised LTβ in several inflammatory cell types in inflammatory myopathies, suggesting its involvement in the different inflammatory mechanisms underlying inflammatory myopathy subgroups.
淋巴毒素β（LTβ）调节一些炎症机制，这些机制可能在特发性炎症性肌病（IM）中起作用。我们通过免疫组织化学、Western blot 和原位杂交研究了炎症性肌病、正常和疾病对照中的 LTβ 和 LTβR。LTβ 存在于正常对照的肌核中，表明其在正常肌肉生理学中的作用。LTβ 在所有肌病的再生肌纤维中强烈上调，但不在去神经的肌纤维中上调。炎症性肌病和肌肉营养不良中的正常肌纤维表达 LTβ，可能反映了早期肌纤维损伤，代表了一个迄今尚未描述的病理标志。此外，我们在炎症性肌病中的几种炎症细胞类型中观察到 LTβ，提示其参与了炎症性肌病亚组不同的炎症机制。
