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Journal of Immunology Research
Volume 2017 (2017), Article ID 5096741, 8 pages
Research Article

IL-1β and IL-6 Are Highly Expressed in RF+IgE+ Systemic Lupus Erythematous Subtype

1Department of Laboratory Medicine, West China Hospital Affiliated to Sichuan University, Chengdu, China
2Department of Rheumatology, West China Hospital Affiliated to Sichuan University, Chengdu, China
3Department of Internal Medicine, Sector Nephrology & Transplantation, Erasmus MC, Rotterdam, Netherlands

Correspondence should be addressed to Lanlan Wang; moc.621@78llgnaw

Received 19 August 2016; Accepted 14 December 2016; Published 12 February 2017

Academic Editor: Nejat K. Egilmez

Copyright © 2017 Yongkang Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Systemic lupus erythematosus (SLE) is an autoimmune disease with great heterogeneity in pathogenesis and clinical symptoms. Rheumatoid factor (RF) is one key indicator for rheumatoid arthritis (RA) while immunoglobulin E (IgE) is associated with type I hypersensitivity. To better categorize SLE subtypes, we determined the dominant cytokines based on familial SLE patients. Methods. RF, IgE, and multiple cytokines (i.e., IL-1β, IL-6, IL-8, IL-10, IL-17, IFN-γ, IP-10, MCP-1, and MIP-1β) were measured in sera of familial SLE patients (), noninherited SLE patients (), and healthy controls (). Results. Three familial SLE patients and 5 noninherited SLE cases are with features of RF+IgE+. These RF+IgE+ SLE patients expressed significantly higher levels of IL-1β and IL-6 than the other SLE patients (). IL-6 correlated with both IgE and IL-1β levels in RF+IgE+ SLE patients (, ; , ), and IgE also correlated with IL-1β (, ). Conclusion. Both IL-1β and IL-6 are highly expressed cytokines in RF+IgE+ SLE subtype which may be related to the pathogenesis of this special SLE subtype and provide accurate treatment strategy by neutralizing IL-1β and IL-6.