Retinal astrocytes respond to IL-17 differently than retinal pigment epithelial cells
AUTOR(ES)
Ke, Yan
FONTE
The Society for Leukocyte Biology
RESUMO
IL-17+ T cells make up the majority of the infiltrating cells in the inflamed eye during the development of EAU. However, the role of IL-17 in ocular inflammation is poorly defined. Given that the primary target cells for IL-17 are parenchymal cells of the tissue, we investigated the in vitro effect of IL-17 on mouse RACs and RPE cells. Our results showed that although RACs and RPE cells expressed the IL-17R, RACs responded to IL-17 by producing increased amounts of proinflammatory cytokines and chemokines, leading to increased migration of granulocytes, whereas RPE cells responded to the same concentration of IL-17 by expressing increased levels of SOCS proteins, resulting in only limited production of proinflammatory cytokines and chemokines and an increased amount of suppressive cytokines, such as LIF. The combination of IL-17 and IFN-γ had a synergistic effect on cell migration with RACs but an antagonistic effect with RPE. In addition, specific inhibitors of the PI3K/Akt signaling pathway completely blocked inflammatory cell migration induced by chemokines released by IL-17-stimulated RACs. Our results demonstrate that IL-17 can induce a pro- or anti-inflammatory effect in the eye, depending on the parenchymal cells stimulated.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2780918Documentos Relacionados
- Endogenous IL-17 contributes to reduced tumor growth and metastasis
- Macrophages and Epithelial Cells Respond Differently to the Pseudomonas aeruginosa Type III Secretion System
- Avaliação da participação de células produtoras de IL-17 (TH17) na paracoccidioidomicose humana : efeito do tratamento com IL-17 e IL-23 sobre a atividade fungicida e capacidade migratória de neutrófilos
- Cloning and characterization of IL-17B and IL-17C, two new members of the IL-17 cytokine family
- Oxidative Stress Renders Retinal Pigment Epithelial Cells Susceptible to Complement-mediated Injury*