AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY 版面费-刊鹿论文编译

What Lies beneath: Preformed Autoantibodies and Lung Transplantation

Abstract:

There is increasing evidence that autoimmunity plays an important role in the progression of chronic lung diseases such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis (1–4). The identification of functionally active (and pathogenic) autoantibodies with specificities for defined self-antigens provides unique insights into the complicated immunology of these disorders, and draws attention to a previously underappreciated pathway involved in the regulation of lung inflammation. Although previous studies have largely focused on the autoantibody repertoires and mechanisms in chronic lung diseases, the potential impact of preexistent autoimmunity in the setting of lung transplantation remains largely unexplored. In this issue of the Journal, Patel and colleagues (pp. 678–686) provide some clues to answering this question (5). Their study extends previous observations that showed the presence of increased concentrations of circulating autoantibodies with specificities for extracellular matrix (ECM) in a 6-month smoking model of emphysema. Patel and colleagues used lungs from smokeexposed mice and non–smoke-exposed controls as donor organs in allogeneic pulmonary transplantations, and found that ischemia/reperfusion injury and antibody/complement deposition were increased in recipients of the smoke-treated allografts. In a subsequent series of unique and clever experiments, the authors further substantiated the impact of preformed autoantibodies by eliminating confounding effects of alloreactivity in a syngeneic lung transplantation model. In these studies, the administration of serum from smoke-exposed mice resulted in increased antibody/complement deposition and lung injury that was clearly independent of allogeneic responses. Moreover, this injury was attenuated when IgG and IgM antibodies were depleted from the smoke-exposed serum. This study adds to prior literature identifying the importance of non-human leukocyte antigen autoantibodies in the pathogenesis of transplant-related lung injury (6, 7). In particular, the current report adds to other evidence that suggests that preformed autoantibodies, which are especially increased in patients with certain chronic lung diseases, contributes to post-transplant allograft dysfunction (8). Although it is provocative, this observation should be considered in a broader context. First, “conventional” autoantibody syndromes are typified by the presence of multiple concurrent specificities, and there is reason to believe that the same holds true in chronic lung diseases. The present study was limited to assessments of anti-ECM autoantibodies, whereas the impact of immunoglobulins with avidities for other lung-specific and extrathoracic autoantigens could be of significant interest. The possibility that the autoreactivity to ECM observed here was due to smoke-induced modifications that rendered self-proteins immunogeneic (i.e., neoantigens) was not explored in this study, although this process may contribute to pathogenic autoreactivity in humans (2). In addition, in most human disorders the various IgG fractions are generally believed to be more pathogenic than IgM, and fractionation and individual transfers of these immunoglobulins might have been enlightening. Furthermore, the development of antibodies against peptide antigens is dependent on the concurrent presence of T-cell reactivity against those same epitopes (9, 10). However, the present study does not shed light on how cellular autoreactivity against ECM (11) or other autoantigens contributes to lung injuries after transplantation. Finally, the longterm impact of these autoantibodies (and autoreactive T cells) was not assessed in this transplant model. It can be predicted that when such studies are performed, they will add considerable value to our understanding of long-term allograft loss. Despite these understandable limitations, this paper provides important insights into post-transplant lung injury. It may have considerable value in providing a template for future studies to further delineate the autoimmunity of post-transplantation allograft injuries. These investigations could include adoptive transfers of autoreactive T cells from smoke-exposed, emphysematous animals, with and without immunoglobulin fractions, to parse out the respective effects of these immune response elements. Perhaps most importantly, the model detailed here, or minor variations of this model, might be a valuable vehicle for preclinical studies of potential therapies. These could include tests of complement inhibitors (12), as the authors mention, or refinements of other modalities focused on autoantibody reduction pretransplantation (13). n

Author Listing： Steven R Duncan;Amit Gaggar

Volume： 60

Pages： 613 - 614

DOI： 10.1165/rcmb.2018-0415ED

Language： English

Journal： American Journal of Respiratory Cell and Molecular Biology

AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY

AM J RESP CELL MOL

影响因子：5.9

是否综述期刊：否

是否OA：否

是否预警：不在预警名单内

发行时间：1989

ISSN：1044-1549

发刊频率：Monthly

收录数据库：SCIE/Scopus收录

出版国家/地区：UNITED STATES

出版社：American Thoracic Society

期刊介绍

The American Journal of Respiratory Cell and Molecular Biology publishes papers that report significant and original observations in the area of pulmonary biology. The focus of the Journal includes, but is not limited to, cellular, biochemical, molecular, developmental, genetic, and immunologic studies of lung cells and molecules.

《美国呼吸细胞和分子生物学杂志》发表的论文报告了肺生物学领域的重要和原始观察结果。该杂志的重点包括但不限于肺细胞和分子的细胞学、生物化学、分子学、发育学、遗传学和免疫学研究。

年发文量	96
国人发稿量	17
国人发文占比	17.71%
自引率	5.1%
平均录取率	较难
平均审稿周期	一般,3-8周
版面费	-
偏重研究方向	生物-呼吸系统
期刊官网	https://www.atsjournals.org/journal/ajrcmb
投稿链接	https://mc.manuscriptcentral.com/ajrcmb

质量指标占比

研究类文章占比	OA被引用占比	撤稿占比	出版后修正文章占比
96.88%	12.42%	0.00%	3.13%

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时间	预警情况
2024年02月发布的2024版	不在预警名单中
2023年01月发布的2023版	不在预警名单中
2021年12月发布的2021版	不在预警名单中
2020年12月发布的2020版	不在预警名单中

JCR分区 WOS分区等级：Q1区

版本	按学科	分区
WOS期刊SCI分区 WOS期刊SCI分区是指SCI官方（Web of Science）为每个学科内的期刊按照IF数值排序，将期刊按照四等分的方法划分的Q1-Q4等级，Q1代表质量最高，即常说的1区期刊。（2021-2022年最新版）
	CELL BIOLOGY	Q1
	RESPIRATORY SYSTEM	Q1
	BIOCHEMISTRY & MOLECULAR BIOLOGY	Q1

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分区表升级版（试行）旨在解决期刊学科体系划分与学科发展以及融合趋势的不相容问题。由于学科交叉在当代科研活动的趋势愈发显著，学科体系构建容易引发争议。为了打破学科体系给期刊评价带来的桎梏，“升级版方案”首先构建了论文层级的主题体系，然后分别计算每篇论文在所属主题的影响力，最后汇总各期刊每篇论文分值，得到“期刊超越指数”，作为分区依据。

分区表升级版（试行）的优势：一是论文层级的主题体系既能体现学科交叉特点，又可以精准揭示期刊载文的多学科性；二是采用“期刊超越指数”替代影响因子指标，解决了影响因子数学性质缺陷对评价结果的干扰。整体而言，分区表升级版（试行）突破了期刊评价中学科体系构建、评价指标选择等瓶颈问题，能够更为全面地揭示学术期刊的影响力，为科研评价“去四唯”提供解决思路。相关研究成果经过国际同行的认可，已经发表在科学计量学领域国际重要期刊。

《2019年中国科学院文献情报中心期刊分区表升级版（试行）》首次将社会科学引文数据库（SSCI）期刊纳入到分区评估中。升级版分区表（试行）设置了包括自然科学和社会科学在内的18个大类学科。基础版和升级版（试行）将过渡共存三年时间，推测在此期间各大高校和科研院所仍可能会以基础版为考核参考标准。提示：中科院分区官方微信公众号“fenqubiao”仅提供基础版数据查询，暂无升级版数据，请注意区分。

中科院分区查看说明

版本	大类学科	小类学科	Top期刊	综述期刊
	医学 1区	CELL BIOLOGY 细胞生物学 2区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	是
2021年12月基础版	医学 2区	CELL BIOLOGY 细胞生物学 3区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	否
2021年12月升级版	医学 1区	CELL BIOLOGY 细胞生物学 2区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	是
2020年12月旧的升级版	医学 1区	CELL BIOLOGY 细胞生物学 2区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	是
2022年12月最新升级版	医学 2区	CELL BIOLOGY 细胞生物学 2区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	否