Th17 cells generated in the absence of TGF-β induce experimental allergic encephalitis upon adoptive transfer

2011 ◽  
Vol 7 (3) ◽  
pp. 283-285 ◽  
Author(s):  
Diego Kyburz ◽  
Maripat Corr
Keyword(s):  
Adoptive Transfer ◽  
Th17 Cells ◽  
Experimental Allergic Encephalitis ◽  
Experimental Allergic

scholarly journals Adoptive transfer of experimental allergic encephalitis

1983 ◽  
Vol 1 (2) ◽  
pp. 162-162
Author(s):  
J. R. Richert ◽  
Marian W. Kies ◽  
E. C. Alvord
Keyword(s):  
Adoptive Transfer ◽  
Experimental Allergic Encephalitis ◽  
Experimental Allergic

scholarly journals GM-CSF mediates autoimmunity by enhancing IL-6–dependent Th17 cell development and survival

2008 ◽  
Vol 205 (10) ◽  
pp. 2281-2294 ◽  
Author(s):  
Ivo Sonderegger ◽  
Giandomenica Iezzi ◽  
Reinhard Maier ◽  
Nicole Schmitz ◽  
Michael Kurrer ◽  
...  
Keyword(s):  
Th17 Cells ◽  
Inflammatory Diseases ◽  
Autoimmune Response ◽  
Gm Csf ◽  
Experimental Allergic Encephalitis ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Experimental Allergic

Granulocyte macrophage–colony stimulating factor (GM-CSF) is critically involved in development of organ-related autoimmune inflammatory diseases including experimental allergic encephalitis and collagen-induced arthritis. Roles of GM-CSF in the initiation and in the effector phase of the autoimmune response have been proposed. Our study was designed to investigate the mechanisms of GM-CSF in autoimmunity using a model of autoimmune heart inflammatory disease (myocarditis). The pathological sequel after immunization with heart myosin has been shown previously to depend on IL-1, IL-6, IL-23, and IL-17. We found that innate GM-CSF was critical for IL-6 and IL-23 responses by dendritic cells and generation of pathological Th17 cells in vivo. Moreover, GM-CSF promoted autoimmunity by enhancing IL-6–dependent survival of antigen specific CD4+ T cells. These results suggest a novel role for GM-CSF in promoting generation and maintenance of Th17 cells by regulation of IL-6 and IL-23 in vivo.

scholarly journals A Novel Role for IL-6 Receptor Classic Signaling: Induction of RORγt+Foxp3+ Tregs with Enhanced Suppressive Capacity

2019 ◽  
Vol 30 (8) ◽  
pp. 1439-1453 ◽  
Author(s):  
Julia Hagenstein ◽  
Simon Melderis ◽  
Anna Nosko ◽  
Matthias T. Warkotsch ◽  
Johannes V. Richter ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Adoptive Transfer ◽  
Th17 Cells ◽  
Inflammatory Diseases ◽  
Double Positive ◽  
T Effector Cells ◽  
Suppressive Capacity

BackgroundNew therapies blocking the IL-6 receptor (IL-6R) have recently become available and are successfully being used to treat inflammatory diseases like arthritis. Whether IL-6 blockers may help patients with kidney inflammation currently remains unknown.MethodsTo learn more about the complex role of CD4+ T cell-intrinsic IL-6R signaling, we induced nephrotoxic nephritis, a mouse model for crescentic GN, in mice lacking T cell–specific IL-6Ra. We used adoptive transfer experiments and studies in reporter mice to analyze immune responses and Treg subpopulations.ResultsLack of IL-6Ra signaling in mouse CD4+ T cells impaired the generation of proinflammatory Th17 cells, but surprisingly did not ameliorate the course of GN. In contrast, renal damage was significantly reduced by restricting IL-6Ra deficiency to T effector cells and excluding Tregs. Detailed studies of Tregs revealed unaltered IL-10 production despite IL-6Ra deficiency. However, in vivo and in vitro, IL-6Ra classic signaling induced RORγt+Foxp3+ double-positive Tregs (biTregs), which carry the trafficking receptor CCR6 and have potent immunoregulatory properties. Indeed, lack of IL-6Ra significantly reduced Treg in vitro suppressive capacity. Finally, adoptive transfer of T cells containing IL-6Ra−/− Tregs resulted in severe aggravation of GN in mice.ConclusionsOur data refine the old paradigm, that IL-6 enhances Th17 responses and suppresses Tregs. We here provide evidence that T cell–intrinsic IL-6Ra classic signaling indeed induces the generation of Th17 cells but at the same time highly immunosuppressive RORγt+ biTregs. These results advocate caution and indicate that IL-6–directed therapies for GN need to be cell-type specific.

The potential role of iNKT cells in experimental allergic encephalitis and multiple sclerosis

2014 ◽  
Vol 36 (2) ◽  
pp. 105-113 ◽  
Author(s):  
Maryam Roozbeh ◽  
Hemn Mohammadpour ◽  
Gholamreza Azizi ◽  
Samira Ghobadzadeh ◽  
Abbas Mirshafiey
Keyword(s):  
Multiple Sclerosis ◽  
Potential Role ◽  
Inkt Cells ◽  
Experimental Allergic Encephalitis ◽  
Experimental Allergic
Sign in / Sign up

Export Citation Format

Share Document