title: IL-19 induced Th2 cytokines and was up-regulated in asthma patients.
abstract: IL-19 belongs to the IL-10 family, which includes IL-10, IL-19, IL-20, IL-22, melanoma differentiation-associated gene-7 (IL-24), and AK155 (IL-26). IL-10 has been shown to inhibit allergen-induced airway hyperreactivity and inflammation. To determine whether IL-19 was also associated with asthma, we used ELISA to analyze the serum level of IL-19 in patients with asthma and found that their serum IL-19 levels were twice those of healthy controls. Patients with a high level of IL-19 also had high levels of IL-4 and IL-13. In a dust mite-induced murine model of asthma, we found that IL-19 level in asthmatic BALB/cJ mice was also twice that of healthy control mice. IL-19 transcript was also induced in the lungs of asthmatic mice. Electroporation i.m. of the IL-19 gene into healthy mice up-regulated IL-4 and IL-5, but not IL-13. However, IL-19 up-regulated IL-13 in asthmatic mice. In vitro, IL-19 induced IL-4, IL-5, IL-10, and IL-13 production by activated T cells. Activation of T cells was required for induction of IL-13 because IL-19 did not induce IL-13 production on nonstimulated T cells. Taken together, these results demonstrated that IL-19 up-regulates Th2 cytokines on activated T cells and might play an important role in the pathogenesis of asthma.
authors.affiliation: Graduate Institute of Biochemistry, National Cheng Kung University, Tainan, Taiwan.
authors.forename: Sheng-Chin
authors.initials: SC
authors.lastname: Liao
authors.forename: Yung-Chih
authors.initials: YC
authors.lastname: Cheng
authors.forename: Yo-Ching
authors.initials: YC
authors.lastname: Wang
authors.forename: Chiung-Wen
authors.initials: CW
authors.lastname: Wang
authors.forename: San-Ming
authors.initials: SM
authors.lastname: Yang
authors.forename: Chun-Keung
authors.initials: CK
authors.lastname: Yu
authors.forename: Chi-Chang
authors.initials: CC
authors.lastname: Shieh
authors.forename: Kuo-Chen
authors.initials: KC
authors.lastname: Cheng
authors.forename: Meng-Feng
authors.initials: MF
authors.lastname: Lee
authors.forename: Shyh-Ren
authors.initials: SR
authors.lastname: Chiang
authors.forename: Jiunn-Min
authors.initials: JM
authors.lastname: Shieh
authors.forename: Ming-Shi
authors.initials: MS
authors.lastname: Chang
mesh_terms: D000328:Adult; D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D016207:Cytokines / Q000096:biosynthesis*; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics / Q000502:physiology*; D018793:Interleukin-13 / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis / Q000097:blood; D015848:Interleukin-5 / Q000096:biosynthesis; D007378:Interleukins; D019169:Jurkat Cells; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology* / Q000378:metabolism*; D014158:Transcription, Genetic; D015854:Up-Regulation / Q000276:immunology*
chemical_list: D016207:Cytokines; C421250:IL19 protein, human; C498891:Il19 protein, mouse; D018793:Interleukin-13; D015848:Interleukin-5; D007378:Interleukins; D016753:Interleukin-10; D015847:Interleukin-4; D007073:Immunoglobulin E