title: IL-10 suppresses Th17 cells and promotes regulatory T cells in the CD4+ T cell population of rheumatoid arthritis patients.
abstract: Interleukin-17-producing CD4(+) T cells (Th17 cells) are the dominant pathogenic cellular component in autoimmune inflammatory diseases, including autoimmune arthritis. IL-10 promotes the generation of Foxp3(+) regulatory T cells via the IL-10 receptor signal. The objective of this study was to examine whether IL-10, which acts as an anti-inflammatory cytokine, has a suppressive effect on the activation of human Th17 cells. Expression of IL-17 and IL-10 was examined immunohistochemically in tissue obtained from rheumatoid arthritis patients. Human peripheral blood CD4(+) T cells were isolated and cultured under various stimulatory conditions. Th17 cells and regulatory T (Treg) cells were detected by flow cytometry. The gene expression of related cytokines and transcription factors were assessed by ELISA and RT-PCR. IL-17 was overexpressed in rheumatoid arthritis patients. IL-10 treatment significantly decreased the numbers of IL-17-producing and RORc-expressing cells among human CD4(+) T cells that had been activated in vitro by Th17-differentiating conditions in autoimmune arthritis patients. IL-10 induced Foxp3(+) regulatory T cells in the human CD4(+) T cell population. Our results demonstrate that IL-17 is overexpressed in autoimmune disease patients and that IL-10 suppresses IL-17 expression. IL-10 may be useful in the treatment of autoimmune diseases.
authors.affiliation: The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul 137-040, South Korea.
authors.forename: Yu-Jung
authors.initials: YJ
authors.lastname: Heo
authors.forename: Young-Bin
authors.initials: YB
authors.lastname: Joo
authors.forename: Hye-Jwa
authors.initials: HJ
authors.lastname: Oh
authors.forename: Mi-Kyung
authors.initials: MK
authors.lastname: Park
authors.forename: Yang-Mi
authors.initials: YM
authors.lastname: Heo
authors.forename: Mi-La
authors.initials: ML
authors.lastname: Cho
authors.forename: Seung-Ki
authors.initials: SK
authors.lastname: Kwok
authors.forename: Ji-Hyeon
authors.initials: JH
authors.lastname: Ju
authors.forename: Kyung-Su
authors.initials: KS
authors.lastname: Park
authors.forename: Seok Goo
authors.initials: SG
authors.lastname: Cho
authors.forename: Sung-Hwan
authors.initials: SH
authors.lastname: Park
authors.forename: Ho-Youn
authors.initials: HY
authors.lastname: Kim
authors.forename: Jun-Ki
authors.initials: JK
authors.lastname: Min
mesh_terms: D001172:Arthritis, Rheumatoid / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D015704:CD4 Antigens / Q000096:biosynthesis; D002478:Cells, Cultured; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D005786:Gene Expression Regulation; D006801:Humans; D007165:Immunosuppression Therapy; D016753:Interleukin-10 / Q000494:pharmacology; D020381:Interleukin-17 / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D008213:Lymphocyte Activation / Q000187:drug effects; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D011994:Recombinant Proteins / Q000494:pharmacology; D013582:Synovial Fluid / Q000166:cytology / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
chemical_list: D015704:CD4 Antigens; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D020381:Interleukin-17; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; C539900:RORC protein, human; D011994:Recombinant Proteins; D016753:Interleukin-10