[HTML][HTML] The IL-6R α chain controls lung CD4+CD25+ Treg development and function during allergic airway inflammation in vivo
A Doganci, T Eigenbrod, N Krug… - The Journal of …, 2005 - Am Soc Clin Investig
A Doganci, T Eigenbrod, N Krug, GT De Sanctis, M Hausding, VJ Erpenbeck, EB Haddad…
The Journal of clinical investigation, 2005•Am Soc Clin InvestigThe cytokine IL-6 acts via a specific receptor complex that consists of the membrane-bound
IL-6 receptor (mIL-6R) or the soluble IL-6 receptor (sIL-6R) and glycoprotein 130 (gp130). In
this study, we investigated the role of IL-6R components in asthma. We observed increased
levels of sIL-6R in the airways of patients with allergic asthma as compared to those in
controls. In addition, local blockade of the sIL-6R in a murine model of late-phase asthma
after OVA sensitization by gp130–fraction constant led to suppression of Th2 cells in the …
IL-6 receptor (mIL-6R) or the soluble IL-6 receptor (sIL-6R) and glycoprotein 130 (gp130). In
this study, we investigated the role of IL-6R components in asthma. We observed increased
levels of sIL-6R in the airways of patients with allergic asthma as compared to those in
controls. In addition, local blockade of the sIL-6R in a murine model of late-phase asthma
after OVA sensitization by gp130–fraction constant led to suppression of Th2 cells in the …
The cytokine IL-6 acts via a specific receptor complex that consists of the membrane-bound IL-6 receptor (mIL-6R) or the soluble IL-6 receptor (sIL-6R) and glycoprotein 130 (gp130). In this study, we investigated the role of IL-6R components in asthma. We observed increased levels of sIL-6R in the airways of patients with allergic asthma as compared to those in controls. In addition, local blockade of the sIL-6R in a murine model of late-phase asthma after OVA sensitization by gp130–fraction constant led to suppression of Th2 cells in the lung. By contrast, blockade of mIL-6R induced local expansion of Foxp3-positive CD4+ CD25+ Tregs with increased immunosuppressive capacities. CD4+ CD25+ but not CD4+ CD25–lung T cells selectively expressed the IL-6R α chain and showed IL-6–dependent STAT-3 phosphorylation. Finally, in an in vivo transfer model of asthma in immunodeficient Rag1 mice, CD4+ CD25+ T cells isolated from anti–IL-6R antibody–treated mice exhibited marked immunosuppressive and antiinflammatory functions. IL-6 signaling therefore controls the balance between effector cells and Tregs in the lung by means of different receptor components. Furthermore, inhibition of IL-6 signaling emerges as a novel molecular approach for the treatment of allergic asthma.
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