特发性炎症性肌病肌组织中腺苷及腺苷受体的分析
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摘要
研究背景和目的
特发性炎症性肌病(ⅡMs)是一组非感染性炎症性肌病,以骨骼肌中炎症细胞浸润及肌纤维萎缩、坏死为主要病理特征,其原因和发生机制不清。以多发性肌炎(PM)、皮肌炎(DM)和包涵体肌炎(IBM)3个亚型最为多见。
腺苷是细胞自分泌或旁分泌途径中的信号分子,在维持内环境稳定方面起重要作用。腺苷可以抑制氧化爆发和肿瘤坏死因子α等炎症因子,在调节免疫和炎症反应方面起重要作用,在败血症患者和克隆恩病动物模型中均发现细胞外腺苷水平升高。腺苷主要通过与其受体结合起作用,腺苷受体检测是判断腺苷发挥抗炎和免疫调节作用的关键环节。
腺苷受体(AR)分四型：A1AR、A2AAR、A2BAR、A3AR,均为G蛋白偶联的七跨膜受体。Lynge J等采用免疫组织化学法和western-blotting法检测人类骨骼肌腺苷受体A,AR、A2AAR和A2BAR的分布,结果观察到骨骼肌仅表达A2BAR和A2AAR肌纤维膜和胞浆中均有表达,而A,AR不表达。1993年Sajjadi FG等采用RT-PCR技术对A3AR进行克隆和序列分析,发现A3AR在人的骨骼肌组织几乎不表达。
细胞外腺苷的来源：一方面,腺苷单磷酸(AMP)在细胞外的5’-核苷酸酶(CD73)作用下脱磷酸产生腺苷。AMP来自于细胞外的腺苷三磷酸(ATP)、腺苷二磷酸(ADP)在三磷酸核苷脱磷酸酶(NTPDase)等作用下脱磷酸生成。细胞外的NTPDases有多种,CD39是细胞外主要的腺苷酸脱磷酸酶,CDML1也是一种常见的细胞外的NTPDase.另一方面,炎性细胞释放腺苷,也是细胞外腺苷的重要来源。
因此,我们检测A2AAR、A2BAR和A3AR在人骨骼肌纤维的表达,IIMs患者肌肉组织腺苷受体表达以及细胞外腺苷生成相关酶表达的变化,探讨腺苷途径作为肌肉组织的自身保护机制在炎症性肌病状态下的改变,为ⅡMs的治疗探索新的方向。
研究对象与方法
选取临床有肌无力症状但肌活检病理无神经肌肉损害表现者17例,四肢来源的骨骼肌14例,竖脊肌3例检测AR表达。收集30例IIMs患者骨骼肌活检组织标本,其中DM患者15例、PM患者11例、IBM患者4例,肌活检大致正常者14例(活检部位均为四肢骨骼肌)作为正常对照,FSHD患者5例作为炎症特异性对照。
对肌活检组织行western印迹分析、免疫组织化学染色,比较ⅡMs患者A2AAR、A2BAR、A3AR以及细胞外腺苷生成相关酶CD73、CD39、CD39L1与正常对照的差别。采用SPSS17.0统计软件进行分析,计量数据以均数±标准差(x±s)表示,统计学分析采用student t检验；分类资料进行x2检验,频数<1时,采用Fisher确切概率法进行分析,检验水平P<0.05。
结果
1.微量肌肉组织Western印迹分析可见A2AAR、A2BAR、A3AR条带。
2.骨骼肌A2AAR、A2BAR和A3AR抗体免疫荧光染色阳性：
A2AAR抗体免疫荧光染色阳性仅见于肌纤维膜,胞浆无明显着色,间质和血管无明显着色；A23AR抗体免疫荧光染色阳性主要见于1型肌纤维胞浆；A3AR抗体免疫荧光染色阳性主要见于2型肌纤维胞浆和血管平滑肌,2型肌纤维胞浆荧光强度+,血管平滑肌荧光强度+++,肌纤维膜无明显着色。
3.Western印迹分析显示3例竖脊肌A2AAR、A2BAR、A3AR条带均较四肢骨骼肌的相应条带宽。
4. IIMs患者非坏死纤维A2AAR、A2BAR和A3AR抗体免疫荧光染色较正常对照增强；western blot分析A2AAR、A2BAR条带灰度值较正常对照增加,A3AR条带灰度值较正常对照无显著差别。部分坏死肌纤维A3AR抗体免疫荧光染色呈强荧光反应。
5.细胞外腺苷生成相关酶CD7。抗体染色见于炎症部位的肌筋膜、肌内膜和部分形态正常肌纤维内膜,非炎症部位的肌间质中也有深染；CD39和CD39L1抗体染色在肌纤维无着色,CD39阳性见于血管内皮细胞,CD39L1阳性见于肌内末梢神经周围和肌梭内。
结论
1.微量肌肉组织Western印迹分析证实人骨骼肌表达A2A、A2B和A3型腺苷受体。
2.A2AAR表达于肌纤维膜,A2BAR主要表达于1型肌纤维胞浆,A3AR表达于2型肌纤维胞浆和血管平滑肌。
3.竖脊肌A2A、A2B和A3型腺苷受体表达量较四肢骨骼肌更高。
4.Western印迹显示IIMs患者A2AR、A2BAR表达增加,A3AR表达不增加；而抗体免疫荧光染色显示IIMs患者非坏死肌纤维A2AAR、A2BAR和A3AR表达均增加,可能与炎症损伤和糖皮质激素应用导致2型肌纤维数量减少有关。
5.A3AR在非坏死肌纤维表达增加且部分坏死肌纤维大量表达提示A3AR可能对细胞的修复和死亡起双向调节作用。
6.CD73主要表达于炎症部位的肌筋膜、肌内膜和血管壁,小血管壁表达增强；非炎症部位的肌筋膜和肌内膜也有表达,正常对照肌间质中仅见大血管内膜和外膜有少量CD73表达,CD73对于IIMs有辅助诊断的作用。
7.CD39表达于肌肉组织血管内皮细胞,CD39L1表达于肌内末梢神经周围和肌梭内,两者在肌纤维表面及胞浆中均无表达,炎症部位与非炎症部位无明显差异。
Background and purpose
Idiopathic inflammatory myopathy (IIMs) is non-infectious inflammatory myopathy, with the main pathological features of the infiltration of inflammatory cells in the skeletal muscle and muscle fiber atrophy and necrosis, the pathogenetic mechanism is still unclear. The most prevalent subtypes are multiple polymyositis (PM), dermatomyositis (DM) and inclusion body myositis (IBM).
The adenosine is the signaling molecule of autocrine or paracrine pathway, and plays an important role in maintaining the internal environment stability. Adenosine can inhibit oxidative burst and tumor necrosis factor-a and other inflammatory cytokines, and is concerned with the regulation of immune and inflammatory responses; it was seen that the extracellular adenosine level was enhanced in patients with sepsis and animal models with Crohn's disease. Adenosine produces its function mainly through binding to its receptor, and adenosine receptor is the key part to detect the anti-inflammatory and immunomodulatory effects of adenosine.
Adenosine receptors (AR) are divided into four types:A1AR, A2AAR, A2BAR, A3AR, and they are all G protein-coupled seven transmembrane receptors. Lynge J et al. used immunohistochemical and western-blotting to detect the distribution of adenosine receptors A1AR, A2AAR, A2BAR in human skeletal muscle, and the result showed that skeletal muscle only expressed A2AAR and A2BAR, both in muscle fiber membrane and cytoplasm, while A1AR was not expressed. In1993, Sajjadi FG et al. used RT-PCR to clone and sequence analysis of A3AR, and found that A3AR was almost not expressed in human skeletal muscle tissue.
Extracellular adenosine Source:a) Adenosine monophosphate (AMP) was dephosphorylated to produce adenosine by the extracellular5'-nucleotidase (CD73). AMP was generated by the extracellular adenosine tri-phosphate (ATP) and adenosine diphosphate (ADP) by nucleoside triphosphates dephosphorylation enzymes (NTPDase). There are several types of extracellular NTPDases, CD39is a major extracellular adenylate dephosphorylation enzyme and CD39L1is also a common extracellular NTPDase. b) The inflammatory cells releasing adenosine is also an important source of the extracellular adenosine.
Therefore, we detected the expression of A2AAR, A2BAR and A3AR in human skeletal muscle fibers, and muscle tissue adenosine receptor expression in the patients with the IIMs, as well as the expression change of extracellular adenosine generation related enzymes, to explore new directions for the treatment of IIMs by exploring the mechanisms of adenosine via its receptor-mediated muscle fibers in inflammatory myopathies state.
Objects of study and methods
In this study, we selected17cases of the patients with the clinical symptoms of myasthenia gravis but no neuromuscular damage performance in muscle biopsy,14cases of the limbs skeletal muscle and3cases of erector spinae was used to detect the AR expression. We collected skeletal muscle biopsy specimens from30IIMs patients, including15patients with dermatomyositis (DM),11patients with polymyositis (PM),4patients with inclusion body myositis (IBM),14cases of normal control (biopsy parts are all limbs skeletal muscle).
We treated the muscle biopsies with western blot analysis and the immunohistochemistry to compare the difference of A2AAR, A2BAR, A3AR and extracellular adenosine generation enzyme CD73, CD39, CD39L1of IMs patients and normal control.Data were described as mean±standard deviation (x±s) and were analyzed using the SPSS17.0statistical software. Comparison between groups were conducted by student t test;classified information was analyzed by χ2test, and Fisher's exact probabilistic method while frequency<1.P value less than0.05was considered statistically significant.
Results
1. Western blot analysis of slight of muscle tissue showed the A2AAR, and A3AR straps.
2. The skeletal muscle A2AAR, A2BAR and A3AR antibody immunofluorescence staining were positive:
A2AAR antibody immune fluorescence staining positive was only found in the muscle fiber membrane, cytoplasm had no obvious coloring, mesenchyme and vascular had no obvious coloring; A2BAR antibody immune fluorescence staining positive was mainly seen in type1muscle fiber cytoplasm; A3AR antibody immune fluorescence staining positive was mainly seen in type2muscle fibers cytoplasm and vascular smooth muscle, the fluorescence intensity of type2muscle fibers cytoplasm:+, the fluorescence intensity of vascular smooth muscle:+++, muscle fiber membrane had no significantly coloring.
3. Western blot analysis showed that the corresponding straps of erector spinae3cases of A2AAR, A2BAR and A3AR were wider than of the limb skeletal muscles.
4. The A2A AR, A2B AR and A3AR antibody immunofluorescence staining in non-necrotic fibers of IIMs patients was enhanced staining compared with normal control; A2AAR, A2BAR straps gray value was increased compared to the normal control, while A3AR strap gray value has no significant difference compared with normal control. A3AR antibody immunofluorescence staining showed strong fluorescence reaction in some necrotic muscle fibers.
5. Extracellular adenosine generation related enzyme CD73antibody staining was seen at fascia musculares and endomysium of the inflammation site and part normal muscle fiber intima, non-inflammation muscle interstitial sites were also deeply stained; CD39and CD39L1antibody staining had no coloring in muscle fibers, while CD39-positive was found in vascular endothelial cells, and CD39L1positive was observed around the intramuscular nerve endings and in the muscle spindle.
Conclusions
1. Western blot analysis of trace amounts of muscle tissue confirmed that human skeletal muscle expressed A2A, A2B and A3type adenosine receptors.
2. A2AAR was expressed in the muscle fiber membrane;A2BAR was mainly expressed in the cytoplasm of type1muscle fibers;A3AR was expressed in the cytoplasm and vascular smooth muscle of type2muscle fibers.
3. The expression of erector spinae A2A, A2B and A3adenosine receptors was higher than that in limb skeletal muscle.
4. Western blot showed that the expression of A2AAR and A2BAR was increased in IIMs patients, while A3AR expression was not increased; the antibody immunofluorescence staining showed that the expression of A2AAR, A2BAR and A3AR was all enhanced in non-necrotic fibers of IIMs patients, which might be concerned with the fact that inflammation injury and the application glucocorticoid hormone lead to the decrease of type2muscle fibers.
5. The expression of A3AR was increased in non-necrotic muscle fibers and some necrotic muscle fibers were highly expressed, which prompted that A3AR might has the two-way adjustment to cell repair and death.
6. CD73was mainly expressed in fascia musculares, endomysium and vascular wall of the inflammation site, and was enhanced in small vessel wall; it was also expressed in fascia musculares and endomysium of non-inflammation site, and there were a small amount of CD73expressed in large endangium and adventitia in mesenchymal of normal control, CD73has the effect to assist diagnosis for IIMs.
7. CD39was expressed in the endothelial cells of the muscle tissues, CD39L1was expressed around the intramuscular nerve endings and in the muscle spindle, but both of them were not expressed in the surface and the cytoplasm of the muscle fibers, non-inflammation sites and inflammation sites had no significant differences.
特发性炎症性肌病(ⅡMs)是一组非感染性炎症性肌病,以骨骼肌中炎症细胞浸润及肌纤维萎缩、坏死为主要病理特征,其原因和发生机制不清。以多发性肌炎(PM)、皮肌炎(DM)和包涵体肌炎(IBM)3个亚型最为多见。
腺苷是细胞自分泌或旁分泌途径中的信号分子,在维持内环境稳定方面起重要作用。腺苷可以抑制氧化爆发和肿瘤坏死因子α等炎症因子,在调节免疫和炎症反应方面起重要作用,在败血症患者和克隆恩病动物模型中均发现细胞外腺苷水平升高。腺苷主要通过与其受体结合起作用,腺苷受体检测是判断腺苷发挥抗炎和免疫调节作用的关键环节。
腺苷受体(AR)分四型：A1AR、A2AAR、A2BAR、A3AR,均为G蛋白偶联的七跨膜受体。Lynge J等采用免疫组织化学法和western-blotting法检测人类骨骼肌腺苷受体A,AR、A2AAR和A2BAR的分布,结果观察到骨骼肌仅表达A2BAR和A2AAR肌纤维膜和胞浆中均有表达,而A,AR不表达。1993年Sajjadi FG等采用RT-PCR技术对A3AR进行克隆和序列分析,发现A3AR在人的骨骼肌组织几乎不表达。
细胞外腺苷的来源：一方面,腺苷单磷酸(AMP)在细胞外的5’-核苷酸酶(CD73)作用下脱磷酸产生腺苷。AMP来自于细胞外的腺苷三磷酸(ATP)、腺苷二磷酸(ADP)在三磷酸核苷脱磷酸酶(NTPDase)等作用下脱磷酸生成。细胞外的NTPDases有多种,CD39是细胞外主要的腺苷酸脱磷酸酶,CDML1也是一种常见的细胞外的NTPDase.另一方面,炎性细胞释放腺苷,也是细胞外腺苷的重要来源。
因此,我们检测A2AAR、A2BAR和A3AR在人骨骼肌纤维的表达,IIMs患者肌肉组织腺苷受体表达以及细胞外腺苷生成相关酶表达的变化,探讨腺苷途径作为肌肉组织的自身保护机制在炎症性肌病状态下的改变,为ⅡMs的治疗探索新的方向。
研究对象与方法
选取临床有肌无力症状但肌活检病理无神经肌肉损害表现者17例,四肢来源的骨骼肌14例,竖脊肌3例检测AR表达。收集30例IIMs患者骨骼肌活检组织标本,其中DM患者15例、PM患者11例、IBM患者4例,肌活检大致正常者14例(活检部位均为四肢骨骼肌)作为正常对照,FSHD患者5例作为炎症特异性对照。
对肌活检组织行western印迹分析、免疫组织化学染色,比较ⅡMs患者A2AAR、A2BAR、A3AR以及细胞外腺苷生成相关酶CD73、CD39、CD39L1与正常对照的差别。采用SPSS17.0统计软件进行分析,计量数据以均数±标准差(x±s)表示,统计学分析采用student t检验；分类资料进行x2检验,频数<1时,采用Fisher确切概率法进行分析,检验水平P<0.05。
结果
1.微量肌肉组织Western印迹分析可见A2AAR、A2BAR、A3AR条带。
2.骨骼肌A2AAR、A2BAR和A3AR抗体免疫荧光染色阳性：
A2AAR抗体免疫荧光染色阳性仅见于肌纤维膜,胞浆无明显着色,间质和血管无明显着色；A23AR抗体免疫荧光染色阳性主要见于1型肌纤维胞浆；A3AR抗体免疫荧光染色阳性主要见于2型肌纤维胞浆和血管平滑肌,2型肌纤维胞浆荧光强度+,血管平滑肌荧光强度+++,肌纤维膜无明显着色。
3.Western印迹分析显示3例竖脊肌A2AAR、A2BAR、A3AR条带均较四肢骨骼肌的相应条带宽。
4. IIMs患者非坏死纤维A2AAR、A2BAR和A3AR抗体免疫荧光染色较正常对照增强；western blot分析A2AAR、A2BAR条带灰度值较正常对照增加,A3AR条带灰度值较正常对照无显著差别。部分坏死肌纤维A3AR抗体免疫荧光染色呈强荧光反应。
5.细胞外腺苷生成相关酶CD7。抗体染色见于炎症部位的肌筋膜、肌内膜和部分形态正常肌纤维内膜,非炎症部位的肌间质中也有深染；CD39和CD39L1抗体染色在肌纤维无着色,CD39阳性见于血管内皮细胞,CD39L1阳性见于肌内末梢神经周围和肌梭内。
结论
1.微量肌肉组织Western印迹分析证实人骨骼肌表达A2A、A2B和A3型腺苷受体。
2.A2AAR表达于肌纤维膜,A2BAR主要表达于1型肌纤维胞浆,A3AR表达于2型肌纤维胞浆和血管平滑肌。
3.竖脊肌A2A、A2B和A3型腺苷受体表达量较四肢骨骼肌更高。
4.Western印迹显示IIMs患者A2AR、A2BAR表达增加,A3AR表达不增加；而抗体免疫荧光染色显示IIMs患者非坏死肌纤维A2AAR、A2BAR和A3AR表达均增加,可能与炎症损伤和糖皮质激素应用导致2型肌纤维数量减少有关。
5.A3AR在非坏死肌纤维表达增加且部分坏死肌纤维大量表达提示A3AR可能对细胞的修复和死亡起双向调节作用。
6.CD73主要表达于炎症部位的肌筋膜、肌内膜和血管壁,小血管壁表达增强；非炎症部位的肌筋膜和肌内膜也有表达,正常对照肌间质中仅见大血管内膜和外膜有少量CD73表达,CD73对于IIMs有辅助诊断的作用。
7.CD39表达于肌肉组织血管内皮细胞,CD39L1表达于肌内末梢神经周围和肌梭内,两者在肌纤维表面及胞浆中均无表达,炎症部位与非炎症部位无明显差异。
Background and purpose
Idiopathic inflammatory myopathy (IIMs) is non-infectious inflammatory myopathy, with the main pathological features of the infiltration of inflammatory cells in the skeletal muscle and muscle fiber atrophy and necrosis, the pathogenetic mechanism is still unclear. The most prevalent subtypes are multiple polymyositis (PM), dermatomyositis (DM) and inclusion body myositis (IBM).
The adenosine is the signaling molecule of autocrine or paracrine pathway, and plays an important role in maintaining the internal environment stability. Adenosine can inhibit oxidative burst and tumor necrosis factor-a and other inflammatory cytokines, and is concerned with the regulation of immune and inflammatory responses; it was seen that the extracellular adenosine level was enhanced in patients with sepsis and animal models with Crohn's disease. Adenosine produces its function mainly through binding to its receptor, and adenosine receptor is the key part to detect the anti-inflammatory and immunomodulatory effects of adenosine.
Adenosine receptors (AR) are divided into four types:A1AR, A2AAR, A2BAR, A3AR, and they are all G protein-coupled seven transmembrane receptors. Lynge J et al. used immunohistochemical and western-blotting to detect the distribution of adenosine receptors A1AR, A2AAR, A2BAR in human skeletal muscle, and the result showed that skeletal muscle only expressed A2AAR and A2BAR, both in muscle fiber membrane and cytoplasm, while A1AR was not expressed. In1993, Sajjadi FG et al. used RT-PCR to clone and sequence analysis of A3AR, and found that A3AR was almost not expressed in human skeletal muscle tissue.
Extracellular adenosine Source:a) Adenosine monophosphate (AMP) was dephosphorylated to produce adenosine by the extracellular5'-nucleotidase (CD73). AMP was generated by the extracellular adenosine tri-phosphate (ATP) and adenosine diphosphate (ADP) by nucleoside triphosphates dephosphorylation enzymes (NTPDase). There are several types of extracellular NTPDases, CD39is a major extracellular adenylate dephosphorylation enzyme and CD39L1is also a common extracellular NTPDase. b) The inflammatory cells releasing adenosine is also an important source of the extracellular adenosine.
Therefore, we detected the expression of A2AAR, A2BAR and A3AR in human skeletal muscle fibers, and muscle tissue adenosine receptor expression in the patients with the IIMs, as well as the expression change of extracellular adenosine generation related enzymes, to explore new directions for the treatment of IIMs by exploring the mechanisms of adenosine via its receptor-mediated muscle fibers in inflammatory myopathies state.
Objects of study and methods
In this study, we selected17cases of the patients with the clinical symptoms of myasthenia gravis but no neuromuscular damage performance in muscle biopsy,14cases of the limbs skeletal muscle and3cases of erector spinae was used to detect the AR expression. We collected skeletal muscle biopsy specimens from30IIMs patients, including15patients with dermatomyositis (DM),11patients with polymyositis (PM),4patients with inclusion body myositis (IBM),14cases of normal control (biopsy parts are all limbs skeletal muscle).
We treated the muscle biopsies with western blot analysis and the immunohistochemistry to compare the difference of A2AAR, A2BAR, A3AR and extracellular adenosine generation enzyme CD73, CD39, CD39L1of IMs patients and normal control.Data were described as mean±standard deviation (x±s) and were analyzed using the SPSS17.0statistical software. Comparison between groups were conducted by student t test;classified information was analyzed by χ2test, and Fisher's exact probabilistic method while frequency<1.P value less than0.05was considered statistically significant.
Results
1. Western blot analysis of slight of muscle tissue showed the A2AAR, and A3AR straps.
2. The skeletal muscle A2AAR, A2BAR and A3AR antibody immunofluorescence staining were positive:
A2AAR antibody immune fluorescence staining positive was only found in the muscle fiber membrane, cytoplasm had no obvious coloring, mesenchyme and vascular had no obvious coloring; A2BAR antibody immune fluorescence staining positive was mainly seen in type1muscle fiber cytoplasm; A3AR antibody immune fluorescence staining positive was mainly seen in type2muscle fibers cytoplasm and vascular smooth muscle, the fluorescence intensity of type2muscle fibers cytoplasm:+, the fluorescence intensity of vascular smooth muscle:+++, muscle fiber membrane had no significantly coloring.
3. Western blot analysis showed that the corresponding straps of erector spinae3cases of A2AAR, A2BAR and A3AR were wider than of the limb skeletal muscles.
4. The A2A AR, A2B AR and A3AR antibody immunofluorescence staining in non-necrotic fibers of IIMs patients was enhanced staining compared with normal control; A2AAR, A2BAR straps gray value was increased compared to the normal control, while A3AR strap gray value has no significant difference compared with normal control. A3AR antibody immunofluorescence staining showed strong fluorescence reaction in some necrotic muscle fibers.
5. Extracellular adenosine generation related enzyme CD73antibody staining was seen at fascia musculares and endomysium of the inflammation site and part normal muscle fiber intima, non-inflammation muscle interstitial sites were also deeply stained; CD39and CD39L1antibody staining had no coloring in muscle fibers, while CD39-positive was found in vascular endothelial cells, and CD39L1positive was observed around the intramuscular nerve endings and in the muscle spindle.
Conclusions
1. Western blot analysis of trace amounts of muscle tissue confirmed that human skeletal muscle expressed A2A, A2B and A3type adenosine receptors.
2. A2AAR was expressed in the muscle fiber membrane;A2BAR was mainly expressed in the cytoplasm of type1muscle fibers;A3AR was expressed in the cytoplasm and vascular smooth muscle of type2muscle fibers.
3. The expression of erector spinae A2A, A2B and A3adenosine receptors was higher than that in limb skeletal muscle.
4. Western blot showed that the expression of A2AAR and A2BAR was increased in IIMs patients, while A3AR expression was not increased; the antibody immunofluorescence staining showed that the expression of A2AAR, A2BAR and A3AR was all enhanced in non-necrotic fibers of IIMs patients, which might be concerned with the fact that inflammation injury and the application glucocorticoid hormone lead to the decrease of type2muscle fibers.
5. The expression of A3AR was increased in non-necrotic muscle fibers and some necrotic muscle fibers were highly expressed, which prompted that A3AR might has the two-way adjustment to cell repair and death.
6. CD73was mainly expressed in fascia musculares, endomysium and vascular wall of the inflammation site, and was enhanced in small vessel wall; it was also expressed in fascia musculares and endomysium of non-inflammation site, and there were a small amount of CD73expressed in large endangium and adventitia in mesenchymal of normal control, CD73has the effect to assist diagnosis for IIMs.
7. CD39was expressed in the endothelial cells of the muscle tissues, CD39L1was expressed around the intramuscular nerve endings and in the muscle spindle, but both of them were not expressed in the surface and the cytoplasm of the muscle fibers, non-inflammation sites and inflammation sites had no significant differences.
引文
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