IL-4 Can Inhibit IL-17 Production in Collagen Induced Arthritis

Authors

  • Huaxi Xu Department of Immunology, Jiangsu University, Zhenjiang, China
  • Samuel Essien Baidoo Department of Immunology, Jiangsu University, Zhenjiang, China
  • Siamak Sandoghchian Shotorbani Department of Immunology, Jiangsu University, Zhenjiang, China | Tabriz Islamic Azad University, Tabriz, Iran
  • Yue Zhang Nanjing Province People Hospital, Nanjing, China
Abstract:

Background: IL-4 is a cytokine that induces differentiation of naive helper T cells into Th2 cells. Once activated by IL-4, Th2 cells subsequently produce additional IL-4. Objective: To examine the effect of IL-4 on IL-17 production and its effect in Collagen- Induced Arthritis (CIA) mice. Method: In this study, a chicken collagen-II-induced experimental arthritis (CIA) model was used in DBA/1 mice to investigate the relationship between IL-4 and IL-17 as well as other inflammatory factors. On the 38th day after the mice were induced with CIA, the expression of IL-17 and IL-4 as well as IFN-γ and IL-13 in sera of the mice was measured by QRT-PCR and ELISA. Result: The result of QRT-PCR analysis of IL-17 and IL-4 mRNA levels in the spleen showed that IL-17 is increased significantly at the onset of CIA in the spleen (p

Upgrade to premium to download articles

Sign up to access the full text

Already have an account?login

similar resources

il-4 can inhibit il-17 production in collagen induced arthritis

background: il-4 is a cytokine that induces differentiation of naive helper t cells into th2 cells. once activated by il-4, th2 cells subsequently produce additional il-4. objective: to examine the effect of il-4 on il-17 production and its effect in collagen- induced arthritis (cia) mice. method: in this study, a chicken collagen-ii-induced experimental arthritis (cia) model was used in dba/1 ...

full text

IL-4 can inhibit IL-17 production in collagen induced arthritis.

BACKGROUND IL-4 is a cytokine that induces differentiation of naive helper T cells into Th2 cells. Once activated by IL-4, Th2 cells subsequently produce additional IL-4. OBJECTIVE To examine the effect of IL-4 on IL-17 production and its effect in Collagen-Induced Arthritis (CIA) mice. METHOD In this study, a chicken collagen-II-induced experimental arthritis (CIA) model was used in DBA/1 ...

full text

IL-17-producing T cells can augment autoantibody-induced arthritis.

Rheumatoid arthritis is a T lymphocyte-mediated disorder, but the precise nature of T cell involvement remains unclear. In the K/BxN mouse model of inflammatory arthritis, T cells initiate disease by providing help to B cells to produce arthritogenic autoantibodies. Here, we have characterized an additional, nonhumoral role for T cells in promoting autoantibody-induced arthritis. Autoreactive K...

full text

Regulation of pathogenic IL-17 responses in collagen-induced arthritis: roles of endogenous interferon-gamma and IL-4

INTRODUCTION Interleukin (IL)-17 plays an important role in the pathogenesis of rheumatoid arthritis and the mouse model collagen-induced arthritis (CIA). Interferon(IFN)-gamma and IL-4 have been shown to suppress Th17 development in vitro, but their potential immunoregulatory roles in vivo are uncertain. The goals of this study were to determine the relationship between Th17 responses and dise...

full text

serum levels of il-17, il-4, and infî³ in serbian patients with early rheumatoid arthritis

background: rheumatoid arthritis (ra) is a chronic, systemic, inflammatory disease with autoimmune etiology, characterized by synovial inflammation and destruction of joint cartilage and bone. there are controversial data about the profile of interleukin-17 (il-17a), interleukin-4 (il-4), and interferon-gamma (infî³), indicating in some studies the key role of il-17, while in others the th1 cyt...

full text

Production of IL-17

Th17 cells are important mediators of autoimmunity, yet the mechanisms by which they are controlled are not fully understood. Studies in mice, including a recent article in Nature Immunology by Yang et al., show that IL-2 is an important inhibitory factor for the differentiation of Th17 cells, inducing phosphorylation of STAT5, which outcompetes STAT3 binding at the IL-17 locus. In humans howev...

full text

My Resources

Save resource for easier access later

Save to my library Already added to my library

{@ msg_add @}


Journal title

volume 8  issue 4

pages  209- 217

publication date 2011-12-01

By following a journal you will be notified via email when a new issue of this journal is published.

Keywords

Hosted on Doprax cloud platform doprax.com

copyright © 2015-2023