Suppr超能文献

B细胞刺激细胞因子BLyS和APRIL在人类牙周炎中升高,并且是实验性小鼠牙周炎中B细胞依赖性骨质流失所必需的。

The B Cell-Stimulatory Cytokines BLyS and APRIL Are Elevated in Human Periodontitis and Are Required for B Cell-Dependent Bone Loss in Experimental Murine Periodontitis.

作者信息

Abe Toshiharu, AlSarhan Mohammed, Benakanakere Manjunatha R, Maekawa Tomoki, Kinane Denis F, Cancro Michael P, Korostoff Jonathan M, Hajishengallis George

机构信息

Department of Microbiology, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104;

Department of Periodontics, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104; and.

出版信息

J Immunol. 2015 Aug 15;195(4):1427-35. doi: 10.4049/jimmunol.1500496. Epub 2015 Jul 6.

Abstract

B-lineage cells (B lymphocytes and plasma cells) predominate in the inflammatory infiltrate of human chronic periodontitis. However, their role in disease pathogenesis and the factors responsible for their persistence in chronic lesions are poorly understood. In this regard, two cytokines of the TNF ligand superfamily, a proliferation-inducing ligand (APRIL) and B-lymphocyte stimulator (BLyS), are important for the survival, proliferation, and maturation of B cells. Thus, we hypothesized that APRIL and/or BLyS are upregulated in periodontitis and contribute to induction of periodontal bone loss. This hypothesis was addressed in both human and mouse experimental systems. We show that, relative to healthy controls, the expression of APRIL and BLyS mRNA and protein was upregulated in natural and experimental periodontitis in humans and mice, respectively. The elevated expression of these cytokines correlated with increased numbers of B cells/plasma cells in both species. Moreover, APRIL and BLyS partially colocalized with κ L chain-expressing B-lineage cells at the epithelial-connective tissue interface. Ligature-induced periodontitis resulted in significantly less bone loss in B cell-deficient mice compared with wild-type controls. Ab-mediated neutralization of APRIL or BLyS diminished the number of B cells in the gingival tissue and inhibited bone loss in wild-type, but not in B cell-deficient, mice. In conclusion, B cells and specific cytokines involved in their growth and differentiation contribute to periodontal bone loss. Moreover, APRIL and BLyS have been identified as potential therapeutic targets in periodontitis.

摘要

B 细胞谱系细胞(B 淋巴细胞和浆细胞)在人类慢性牙周炎的炎症浸润中占主导地位。然而,它们在疾病发病机制中的作用以及导致它们在慢性病变中持续存在的因素却知之甚少。在这方面,肿瘤坏死因子配体超家族的两种细胞因子,增殖诱导配体(APRIL)和 B 淋巴细胞刺激因子(BLyS),对 B 细胞的存活、增殖和成熟很重要。因此,我们假设 APRIL 和/或 BLyS 在牙周炎中上调,并导致牙周骨丧失。在人类和小鼠实验系统中都对这一假设进行了验证。我们发现,与健康对照相比,APRIL 和 BLyS 的 mRNA 和蛋白表达在人类和小鼠的自然和实验性牙周炎中分别上调。这些细胞因子的表达升高与两个物种中 B 细胞/浆细胞数量的增加相关。此外,APRIL 和 BLyS 在上皮-结缔组织界面与表达 κ 轻链的 B 细胞谱系细胞部分共定位。与野生型对照相比,结扎诱导的牙周炎在 B 细胞缺陷小鼠中导致的骨丧失明显更少。抗体介导的 APRIL 或 BLyS 中和减少了牙龈组织中 B 细胞的数量,并抑制了野生型小鼠(而非 B 细胞缺陷小鼠)的骨丧失。总之,参与 B 细胞生长和分化的 B 细胞和特定细胞因子导致了牙周骨丧失。此外,APRIL 和 BLyS 已被确定为牙周炎的潜在治疗靶点。

相似文献

4
Preliminary findings on the possible role of B-lymphocyte stimulator (BLyS) on diabetes-related periodontitis.
Braz Oral Res. 2020 Apr 30;34:e038. doi: 10.1590/1807-3107bor-2020.vol34.0038. eCollection 2020.
5
Human gingival fibroblasts are a source of B cell-activating factor during periodontal inflammation.
J Periodontol. 2024 Jul;95(7):673-681. doi: 10.1002/JPER.23-0543. Epub 2023 Dec 13.
6
APRIL/BLyS Blockade Reduces Donor-specific Antibodies in Allosensitized Mice.
Transplantation. 2019 Jul;103(7):1372-1384. doi: 10.1097/TP.0000000000002686.
7
Intrarenal production of B-cell survival factors in human lupus nephritis.
Mod Pathol. 2011 Jan;24(1):98-107. doi: 10.1038/modpathol.2010.184. Epub 2010 Oct 1.
9
In vitro and in vivo activation induces BAFF and APRIL expression in B cells.
J Immunol. 2007 Nov 1;179(9):5947-57. doi: 10.4049/jimmunol.179.9.5947.

引用本文的文献

2
Comparative Analysis of Salivary and Serum Inflammatory Mediator Profiles in Patients With Rheumatoid Arthritis and Periodontitis.
Mediators Inflamm. 2025 Mar 20;2025:7739833. doi: 10.1155/mi/7739833. eCollection 2025.
4
Causal relationship between immune cells and periodontitis: A Mendelian randomization study.
Medicine (Baltimore). 2024 Dec 13;103(50):e40918. doi: 10.1097/MD.0000000000040918.
5
Gingival spatial analysis reveals geographic immunological variation in a microbiota-dependent and -independent manner.
NPJ Biofilms Microbiomes. 2024 Dec 3;10(1):142. doi: 10.1038/s41522-024-00625-2.
6
Comprehensive Analysis of Sialylation-Related Gene Profiles and Their Impact on the Immune Microenvironment in Periodontitis.
Inflammation. 2025 Aug;48(4):2087-2104. doi: 10.1007/s10753-024-02177-1. Epub 2024 Nov 29.
8
Th17-to-Tfh plasticity during periodontitis limits disease pathology.
J Exp Med. 2024 Aug 5;221(8). doi: 10.1084/jem.20232015. Epub 2024 May 31.
9
Immune cell composition and inflammatory profile of human peri-implantitis and periodontitis lesions.
Clin Exp Immunol. 2024 Jul 12;217(2):173-182. doi: 10.1093/cei/uxae033.
10
Illuminating the oral microbiome and its host interactions: animal models of disease.
FEMS Microbiol Rev. 2023 May 19;47(3). doi: 10.1093/femsre/fuad018.

本文引用的文献

1
The enduring importance of animal models in understanding periodontal disease.
Virulence. 2015;6(3):229-35. doi: 10.4161/21505594.2014.990806.
2
Periodontitis: from microbial immune subversion to systemic inflammation.
Nat Rev Immunol. 2015 Jan;15(1):30-44. doi: 10.1038/nri3785.
3
Polymicrobial synergy and dysbiosis in inflammatory disease.
Trends Mol Med. 2015 Mar;21(3):172-83. doi: 10.1016/j.molmed.2014.11.004. Epub 2014 Nov 20.
4
Cellular composition of long-standing gingivitis and periodontitis lesions.
J Periodontal Res. 2015 Aug;50(4):535-43. doi: 10.1111/jre.12236. Epub 2014 Oct 20.
5
Periodontitis in the absence of B cells and specific anti-bacterial antibody.
Mol Oral Microbiol. 2015 Apr;30(2):160-9. doi: 10.1111/omi.12082. Epub 2014 Oct 28.
6
Regulation of osteoclast homeostasis and inflammatory bone loss by MFG-E8.
J Immunol. 2014 Aug 1;193(3):1383-91. doi: 10.4049/jimmunol.1400970. Epub 2014 Jun 23.
7
Genetic and intervention studies implicating complement C3 as a major target for the treatment of periodontitis.
J Immunol. 2014 Jun 15;192(12):6020-7. doi: 10.4049/jimmunol.1400569. Epub 2014 May 7.
8
B cells promote obesity-associated periodontitis and oral pathogen-associated inflammation.
J Leukoc Biol. 2014 Aug;96(2):349-57. doi: 10.1189/jlb.4A0214-095R. Epub 2014 Apr 29.
9
The BAFF/APRIL system in SLE pathogenesis.
Nat Rev Rheumatol. 2014 Jun;10(6):365-73. doi: 10.1038/nrrheum.2014.33. Epub 2014 Mar 11.
10
Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response.
Trends Immunol. 2014 Jan;35(1):3-11. doi: 10.1016/j.it.2013.09.001. Epub 2013 Oct 23.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验