title: IL-37 inhibits the production of inflammatory cytokines in peripheral blood mononuclear cells of patients with systemic lupus erythematosus: its correlation with disease activity.
abstract: BACKGROUND
  Interleukin-37 (IL-37), a new member of IL-1 family cytokine, is recently identified as a natural inhibitor of innate immunity. This study aimed to measure the peripheral blood mononuclear cells (PBMCs) and serum levels of IL-37 in patients with systemic lupus erythematosus (SLE) and to investigate its role in SLE, including its correlation with disease activity, organ disorder and the regulation of inflammatory cytokines.
  
  
  METHODS
  The expressions of IL-37 mRNAs in PBMCs and serum IL-37 levels in 66 SLE patients were measured by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). SLE patients PBMCs were stimulated with recombinant IL-37, levels of cytokines TNF-α, IL-1β, IL-6 and IL-10 were detected by RT-PCR and ELISA.
  
  
  RESULTS
  IL-37 mRNAs and serum protein levels were higher in patients with SLE compared with healthy controls. Patients with active disease showed higher IL-37 mRNAs and serum protein levels compared with those with inactive disease as well as healthy controls. Serum IL-37 levels correlated with SLEDAI and inversely with C3 and C4. Serum IL-37 levels were higher in SLE patients with renal involvement compared with those without renal disease. In vitro, IL-37 inhibited the production of TNF-α, IL-1β and IL-6 in PBMCs of patients with SLE, whereas the production of IL-10 was unaffected.
  
  
  CONCLUSIONS
  IL-37 associated with SLE disease activity, especially related with SLE renal disease activity. IL-37 is an important cytokine in the control of SLE pathogenesis by suppressing the production of inflammatory cytokines. Thus, IL-37 may provide a novel research target for the pathogenesis and therapy of SLE.
authors.forename: Liang
authors.initials: L
authors.lastname: Ye
authors.forename: Ling
authors.initials: L
authors.lastname: Ji
authors.forename: Zhongyang
authors.initials: Z
authors.lastname: Wen
authors.forename: Yanfei
authors.initials: Y
authors.lastname: Zhou
authors.forename: Dongsheng
authors.initials: D
authors.lastname: Hu
authors.forename: Yanqun
authors.initials: Y
authors.lastname: Li
authors.forename: Ting
authors.initials: T
authors.lastname: Yu
authors.forename: Bingni
authors.initials: B
authors.lastname: Chen
authors.forename: Jinshun
authors.initials: J
authors.lastname: Zhang
authors.forename: Liping
authors.initials: L
authors.lastname: Ding
authors.affiliation: Biological therapy institute, Shenzhen University School of Medicine, 518060 Shenzhen, China. dujing83@hotmail.com.
authors.forename: Jing
authors.initials: J
authors.lastname: Du
authors.forename: Zhong
authors.initials: Z
authors.lastname: Huang
mesh_terms: D000293:Adolescent; D000328:Adult; D001798:Blood Proteins / Q000378:metabolism; D016022:Case-Control Studies; D016207:Cytokines / Q000096:biosynthesis / Q000097:blood*; D003710:Demography; D018450:Disease Progression; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D007375:Interleukin-1 / Q000097:blood* / Q000235:genetics; D007668:Kidney / Q000187:drug effects / Q000473:pathology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism*; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000235:genetics / Q000276:immunology / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000494:pharmacology; D055815:Young Adult
chemical_list: D001798:Blood Proteins; D016207:Cytokines; C508587:IL37 protein, human; D018836:Inflammation Mediators; D007375:Interleukin-1; D012333:RNA, Messenger; D011993:Recombinant Fusion Proteins