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IL-23 promotes CD4+ T cells to produce IL-17 in Vogt-Koyanagi-Harada disease.
J Allergy Clin Immunol. 2007 May; 119(5):1218-24.JA

Abstract

BACKGROUND

Vogt-Koyanagi-Harada (VKH) disease is a systemic refractory autoimmune disease. IL-23 has been thought to play a critical role in autoimmune disease through inducing the development of IL-17-producing CD4(+) T cells.

OBJECTIVE

To investigate the expression of IL-23 and IL-17 and the influence of IL-23 on IL-17 production in patients with VKH disease.

METHODS

Blood samples were taken from 25 patients with VKH disease and 16 healthy controls. Peripheral blood mononuclear cells (PBMCs) were subjected to analysis of IL-23p19 mRNA and IL-23 protein expression using RT-PCR and ELISA, respectively. The IL-17 levels in the supernatants of PBMCs and CD4(+) T cells cultured in the absence or presence of recombinant (r)IL-23, rIL-12, or anti-IFN-gamma were determined by ELISA.

RESULTS

The patients with VKH disease with active uveitis showed an elevated level of IL-23p19 mRNA in PBMCs, higher IL-23 in the serum and supernatants of PBMCs, and increased production of IL-17 by polyclonally stimulated PBMCs and CD4(+) T cells. Recombinant IL-23 significantly enhanced IL-17 production, whereas rIL-12 and IFN-gamma inhibited IL-17 production. More importantly, IL-17 production was significantly increased in patients with active uveitis in the presence of rIL-23. Both rIL-23 and rIL-12 enhanced IFN-gamma production.

CONCLUSION

The results suggest that IL-23-stimulated production of IL-17 by CD4(+) T cells may be responsible for the development of uveitis seen in patients with VKH disease.

CLINICAL IMPLICATIONS

This study provides a new insight into the mechanism involved in the development of VKH disease.

Authors+Show Affiliations

State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Uveitis Study Center, Sun Yat-sen University, Guanzhou, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

17335887

Citation

Chi, Wei, et al. "IL-23 Promotes CD4+ T Cells to Produce IL-17 in Vogt-Koyanagi-Harada Disease." The Journal of Allergy and Clinical Immunology, vol. 119, no. 5, 2007, pp. 1218-24.
Chi W, Yang P, Li B, et al. IL-23 promotes CD4+ T cells to produce IL-17 in Vogt-Koyanagi-Harada disease. J Allergy Clin Immunol. 2007;119(5):1218-24.
Chi, W., Yang, P., Li, B., Wu, C., Jin, H., Zhu, X., Chen, L., Zhou, H., Huang, X., & Kijlstra, A. (2007). IL-23 promotes CD4+ T cells to produce IL-17 in Vogt-Koyanagi-Harada disease. The Journal of Allergy and Clinical Immunology, 119(5), 1218-24.
Chi W, et al. IL-23 Promotes CD4+ T Cells to Produce IL-17 in Vogt-Koyanagi-Harada Disease. J Allergy Clin Immunol. 2007;119(5):1218-24. PubMed PMID: 17335887.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - IL-23 promotes CD4+ T cells to produce IL-17 in Vogt-Koyanagi-Harada disease. AU - Chi,Wei, AU - Yang,Peizeng, AU - Li,Bing, AU - Wu,Changyou, AU - Jin,Haoli, AU - Zhu,Xuefei, AU - Chen,Lina, AU - Zhou,Hongyan, AU - Huang,Xiangkun, AU - Kijlstra,Aize, Y1 - 2007/03/01/ PY - 2006/11/06/received PY - 2007/01/09/revised PY - 2007/01/09/accepted PY - 2007/3/6/pubmed PY - 2007/7/7/medline PY - 2007/3/6/entrez SP - 1218 EP - 24 JF - The Journal of allergy and clinical immunology JO - J. Allergy Clin. Immunol. VL - 119 IS - 5 N2 - BACKGROUND: Vogt-Koyanagi-Harada (VKH) disease is a systemic refractory autoimmune disease. IL-23 has been thought to play a critical role in autoimmune disease through inducing the development of IL-17-producing CD4(+) T cells. OBJECTIVE: To investigate the expression of IL-23 and IL-17 and the influence of IL-23 on IL-17 production in patients with VKH disease. METHODS: Blood samples were taken from 25 patients with VKH disease and 16 healthy controls. Peripheral blood mononuclear cells (PBMCs) were subjected to analysis of IL-23p19 mRNA and IL-23 protein expression using RT-PCR and ELISA, respectively. The IL-17 levels in the supernatants of PBMCs and CD4(+) T cells cultured in the absence or presence of recombinant (r)IL-23, rIL-12, or anti-IFN-gamma were determined by ELISA. RESULTS: The patients with VKH disease with active uveitis showed an elevated level of IL-23p19 mRNA in PBMCs, higher IL-23 in the serum and supernatants of PBMCs, and increased production of IL-17 by polyclonally stimulated PBMCs and CD4(+) T cells. Recombinant IL-23 significantly enhanced IL-17 production, whereas rIL-12 and IFN-gamma inhibited IL-17 production. More importantly, IL-17 production was significantly increased in patients with active uveitis in the presence of rIL-23. Both rIL-23 and rIL-12 enhanced IFN-gamma production. CONCLUSION: The results suggest that IL-23-stimulated production of IL-17 by CD4(+) T cells may be responsible for the development of uveitis seen in patients with VKH disease. CLINICAL IMPLICATIONS: This study provides a new insight into the mechanism involved in the development of VKH disease. SN - 0091-6749 UR - https://www.unboundmedicine.com/medline/citation/17335887/IL_23_promotes_CD4+_T_cells_to_produce_IL_17_in_Vogt_Koyanagi_Harada_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0091-6749(07)00169-8 DB - PRIME DP - Unbound Medicine ER -