本期AJRCCM有不少好文章！
CD48 Is Critically Involved in Allergic Eosinophilic Airway Inflammation
Ariel Munitz
Rationale: Despite ongoing research, the molecular mechanisms controlling asthma are still elusive. CD48 is a glycosylphosphatidylinositol-anchored protein involved in lymphocyte adhesion, activation, and costimulation. Although CD48 is widely expressed on hematopoietic cells and commonly studied in the context of natural killer and cytotoxic T cell functions, its role in helper T cell type 2 settings has not been examined.
Objectives: To evaluate the expression and function of CD48, CD2, and 2B4 in a murine model of allergic eosinophilic airway inflammation.
Methods: Allergic eosinophilic airway inflammation was induced by ovalbumin (OVA)–alum sensitization and intranasal inoculation of OVA or, alternatively, by repeated intranasal inoculation of Aspergillus fumigatus antigen in wild-type, STAT (signal transducer and activator of transcription)-6–deficient, and IL-4/IL-13–deficient BALB/c mice. Gene profiling of whole lungs was performed, followed by Northern blot and flow cytometric analysis. Anti-CD48, -CD2, and -2B4 antibodies were administered before OVA challenge and cytokine expression and histology were assessed.
Measurements and Main Results: Microarray data analysis demonstrated upregulation of CD48 in the lungs of OVA-challenged mice. Allergen-induced CD48 expression was independent of STAT-6, IL-13, and IL-4. Neutralization of CD48 in allergen-challenged mice abrogated bronchoalveolar lavage fluid and lung inflammation. Neutralization of CD2 inhibited the inflammatory response to a lesser extent and neutralization of 2B4 had no effect.
Conclusions: Our results suggest that CD48 is critically involved in allergic eosinophilic airway inflammation. As such, CD48 may provide a new potential target for the suppression of asthma.
Key Words: asthma • CD48 • CD2 • 2B4
AT A GLANCE COMMENTARY
Scientific Knowledge on the Subject
CD48 is an activation molecule able to facilitate various cellular activities. Its role in asthma is unknown.
What This Study Adds to the Field
CD48 is upregulated in experimental asthma. Anti-CD48–based therapies may be useful for asthma and perhaps various allergic diseases.
American Journal of Respiratory and Critical Care Medicine Vol 175. pp. 911-918, (2007)
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D48 Is Critically Involved in Allergic Eosinophilic Airway Inflammation
标题：CD48因子与气道嗜酸性过敏炎症反应加重有关
Rationale: Despite ongoing research, the molecular mechanisms controlling asthma are still elusive. CD48 is a glycosylphosphatidylinositol-anchored protein involved in lymphocyte adhesion, activation, and costimulation. Although CD48 is widely expressed on hematopoietic cells and commonly studied in the context of natural killer and cytotoxic T cell functions, its role in helper T cell type 2 settings has not been examined.
背景；尽管进行了（一系列）研究，但是（决定）哮喘发病的分子机制仍然不明。CD48因子是一种与淋巴细胞的黏附，激活和聚集有关的一种以糖基磷脂酰肌醇为靶点的蛋白质。尽管CD48因子广泛表达于造血细胞并且在自然杀伤细胞和细胞毒T淋巴细胞的功能研究中广泛涉及，但是它在2型辅助性T 淋巴细胞中的作用还未得到证实。
Objectives: To evaluate the expression and function of CD48, CD2, and 2B4 in a murine model of allergic eosinophilic airway inflammation.
目的：测定CD48, CD2, 和 2B4因子在鼠气道嗜酸性过敏炎症反应模型中的表达和作用。
Methods: Allergic eosinophilic airway inflammation was induced by ovalbumin (OVA)–alum sensitization and intranasal inoculation of OVA or, alternatively, by repeated intranasal inoculation of Aspergillus fumigatus antigen in wild-type, STAT (signal transducer and activator of transcription)-6–deficient, and IL-4/IL-13–deficient BALB/c mice. Gene profiling of whole lungs was performed, followed by Northern blot and flow cytometric analysis. Anti-CD48, -CD2, and -2B4 antibodies were administered before OVA challenge and cytokine expression and histology were assessed.
方法：在野生型，STAT（信号转导，激活和转录）因子6缺失和白介素4和13缺失的BALB/c系小鼠，鼻内接种铝致敏的卵清蛋白或替代性鼻内接种野生型烟曲病抗原来诱发气道嗜酸性过敏炎症反应。应用RNA印迹技术和流式细胞仪检测分析全肺的基因（表达）。在接种卵清蛋白，细胞因子和组织学测定前，（在小鼠中）应用抗CD48, CD2, 和 2B4抗体。
Measurements and Main Results: Microarray data analysis demonstrated upregulation of CD48 in the lungs of OVA-challenged mice. Allergen-induced CD48 expression was independent of STAT-6, IL-13, and IL-4. Neutralization of CD48 in allergen-challenged mice abrogated bronchoalveolar lavage fluid and lung inflammation. Neutralization of CD2 inhibited the inflammatory response to a lesser extent and neutralization of 2B4 had no effect.
结果；在接种卵清蛋白的小鼠的肺中应用微点阵分析表明，CD48 因子（表达）上调。过敏原诱发的CD48表达与STAT因子6，白介素13和白介素4因子无关。降低过敏原致敏的小鼠的CD48因子（水平）可以减少支气管肺泡灌洗液（用量）和肺炎症反应。降低 CD2因子（水平）可以使（气道）炎症反应减小到更小的范围。降低 2B4水平，（对炎症反应）无明显作用。
Conclusions: Our results suggest that CD48 is critically involved in allergic eosinophilic airway inflammation. As such, CD48 may provide a new potential target for the suppression of asthma.
结论；结果表明， CD48因子加重气道嗜酸性过敏炎症反应。由此（我们得出），CD48因子可能提供一种新的有潜力的（治疗）目标。
Key Words: asthma ? CD48 ? CD2 ? 2B4
关键词：哮喘， CD48 ，CD2 ，2B4
AT A GLANCE COMMENTARY
Scientific Knowledge on the Subject
CD48 is an activation molecule able to facilitate various cellular activities. Its role in asthma is unknown.
短评：此研究的科学意义
CD48因子是一种能促进不同细胞活动的激活分子。但它在哮喘中的作用还未明确。
What This Study Adds to the Field
CD48 is upregulated in experimental asthma. Anti-CD48–based therapies may be useful for asthma and perhaps various allergic diseases.
此研究对临床的帮助
CD48因子加重（实验性）哮喘发作。以抗CD48因子为基础的治疗措施可能有助于哮喘和其他过敏性疾病的治疗。
American Journal of Respiratory and Critical Care Medicine Vol 175. pp. 911-918, (2007)
美国呼吸和急症医学，2007，175：911-918
编译：CD48因子加重气道嗜酸性过敏炎症反应
背景：哮喘发病的分子机制迄今不明。CD48因子是一种与淋巴细胞的黏附，激活和聚集有关的一种以糖基磷脂酰肌醇为靶点的蛋白质。尽管CD48因子广泛表达于造血细胞并且在自然杀伤细胞和细胞毒T淋巴细胞的功能研究中广泛涉及，但是它在2型辅助性T 淋巴细胞中的作用还未得到证实。
目的：测定CD48, CD2, 和 2B4因子在鼠气道嗜酸性过敏炎症反应模型中的表达和作用。
方法：在野生型，STAT（信号转导，激活和转录）因子6缺失和白介素4和13缺失的BALB/c系小鼠，鼻内接种铝致敏的卵清蛋白或替代性鼻内接种野生型烟曲病抗原来诱发气道嗜酸性过敏炎症反应。应用RNA印迹技术和流式细胞仪检测分析全肺的基因（表达）。在接种卵清蛋白，细胞因子和组织学测定前，在小鼠模型中应用抗CD48, CD2, 和 2B4抗体。
结果：在接种卵清蛋白的小鼠的肺中应用微点阵分析表明，CD48 因子的（表达）上调。过敏原诱发的CD48表达与STAT因子6，白介素13和白介素4因子无关。降低过敏原致敏的小鼠的CD48因子（水平）可以减少支气管肺泡灌洗液（用量）和肺炎症反应。降低 CD2因子（水平）可以使（气道）炎症反应减小到更小的范围。降低 2B4水平，（对炎症反应）无明显作用。
结论：CD48因子加重气道嗜酸性过敏炎症反应，CD48因子可能提供一种新的有潜力的（治疗)目标。
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