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High-throughput RNA sequencing reveals distinct gene signatures in active IgG4-related disease.
Sci Rep 2017; 7(1):17567SR

Abstract

We aimed to characterize the molecular differences and effects from prednisone treatment among IgG4-related disease with salivary gland lesions (RD-SG), without SG lesions (RD-nonSG), and IgG4-related retroperitoneal fibrosis (RF). RNA sequencing was conducted on blood from 25 RD-SG, 11 RD-nonSG, 3 RF and 10 control subjects. Among these, 8 RD-nonSG and 12 RD-SG patients were subjected to treatment with prednisone and/or glucocorticoid-sparing agents. Six RD patients had a longitudinal time point. The mRNA levels of IgG4 and IgE, genes specific for Th2 cells, eosinophils, and neutrophils were over-expressed in RD-SG and RD-nonSG. A B-cell signature was suppressed in patients group versus controls, while Th1, Th2, Treg, and eosinophil gene signatures were increased in patients without treatment. Interestingly, Tfh genes and B cell signature were decreased at flare disease state. Prednisone treatment led to increased neutrophil, but decreased Treg signatures. Serum IgG4 levels correlated with the eosinophil and neutrophil gene signatures in RD-SG patients, and with a B cell signature in only RD-nonSG patients. IgG4, IgE, and cell-specific signatures are regulated in patients, suggesting the imbalance of immune and inflammatory cells in IgG4-related disease. Prednisone treatment selectively modulates Treg, eosinophil, and neutrophil signatures.

Authors+Show Affiliations

MedImmune, Gaithersburg, MD, 20878, USA.Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing, 100044, China.Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing, 100044, China.MedImmune, Gaithersburg, MD, 20878, USA.MedImmune, Gaithersburg, MD, 20878, USA.MedImmune, Gaithersburg, MD, 20878, USA.Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing, 100044, China.Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing, 100044, China.Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing, 100044, China.Department of Oral and Maxillofacial Surgery, Peking University School of Stomatology, Beijing, 100081, China.Department of Immunology and Rheumatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430000, China.Department of Oral Medicine, Peking University School of Stomatology, Beijing, 100081, China.Department of Oral Medicine, Peking University School of Stomatology, Beijing, 100081, China.Department of Radiology, Peking University People's Hospital, Beijing, 100044, China.Department of Rheumatology and Immunology, Beijing Tongren Hospital, Beijing, 1000730, China.MedImmune, Gaithersburg, MD, 20878, USA. yaoy@medimmune.com.Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing, 100044, China. zgli99@aliyun.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29242501

Citation

Higgs, Brandon W., et al. "High-throughput RNA Sequencing Reveals Distinct Gene Signatures in Active IgG4-related Disease." Scientific Reports, vol. 7, no. 1, 2017, p. 17567.
Higgs BW, Liu Y, Guo J, et al. High-throughput RNA sequencing reveals distinct gene signatures in active IgG4-related disease. Sci Rep. 2017;7(1):17567.
Higgs, B. W., Liu, Y., Guo, J., Sebastian, Y., Morehouse, C., Zhu, W., ... Li, Z. G. (2017). High-throughput RNA sequencing reveals distinct gene signatures in active IgG4-related disease. Scientific Reports, 7(1), p. 17567. doi:10.1038/s41598-017-17602-9.
Higgs BW, et al. High-throughput RNA Sequencing Reveals Distinct Gene Signatures in Active IgG4-related Disease. Sci Rep. 2017 12 14;7(1):17567. PubMed PMID: 29242501.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - High-throughput RNA sequencing reveals distinct gene signatures in active IgG4-related disease. AU - Higgs,Brandon W, AU - Liu,Yanying, AU - Guo,Jianping, AU - Sebastian,Yinong, AU - Morehouse,Chris, AU - Zhu,Wei, AU - Ren,Limin, AU - Liu,Mengru, AU - Du,Yan, AU - Yu,Guangyan, AU - Dong,Lingli, AU - Hua,Hong, AU - Wei,Pan, AU - Wang,Yi, AU - Wang,Zhengang, AU - Yao,Yihong, AU - Li,Zhan-Guo, Y1 - 2017/12/14/ PY - 2017/07/04/received PY - 2017/11/29/accepted PY - 2017/12/16/entrez PY - 2017/12/16/pubmed PY - 2017/12/16/medline SP - 17567 EP - 17567 JF - Scientific reports JO - Sci Rep VL - 7 IS - 1 N2 - We aimed to characterize the molecular differences and effects from prednisone treatment among IgG4-related disease with salivary gland lesions (RD-SG), without SG lesions (RD-nonSG), and IgG4-related retroperitoneal fibrosis (RF). RNA sequencing was conducted on blood from 25 RD-SG, 11 RD-nonSG, 3 RF and 10 control subjects. Among these, 8 RD-nonSG and 12 RD-SG patients were subjected to treatment with prednisone and/or glucocorticoid-sparing agents. Six RD patients had a longitudinal time point. The mRNA levels of IgG4 and IgE, genes specific for Th2 cells, eosinophils, and neutrophils were over-expressed in RD-SG and RD-nonSG. A B-cell signature was suppressed in patients group versus controls, while Th1, Th2, Treg, and eosinophil gene signatures were increased in patients without treatment. Interestingly, Tfh genes and B cell signature were decreased at flare disease state. Prednisone treatment led to increased neutrophil, but decreased Treg signatures. Serum IgG4 levels correlated with the eosinophil and neutrophil gene signatures in RD-SG patients, and with a B cell signature in only RD-nonSG patients. IgG4, IgE, and cell-specific signatures are regulated in patients, suggesting the imbalance of immune and inflammatory cells in IgG4-related disease. Prednisone treatment selectively modulates Treg, eosinophil, and neutrophil signatures. SN - 2045-2322 UR - https://www.unboundmedicine.com/medline/citation/29242501/High_throughput_RNA_sequencing_reveals_distinct_gene_signatures_in_active_IgG4_related_disease_ L2 - http://dx.doi.org/10.1038/s41598-017-17602-9 DB - PRIME DP - Unbound Medicine ER -