Interleukin 17–producing T helper cells and interleukin 17 orchestrate autoreactive germinal center development in autoimmune BXD2 mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-12-23

AUTHORS

Hui-Chen Hsu, PingAr Yang, John Wang, Qi Wu, Riley Myers, Jian Chen, John Yi, Tanja Guentert, Albert Tousson, Andrea L Stanus, Thuc-vy L Le, Robin G Lorenz, Hui Xu, Jay K Kolls, Robert H Carter, David D Chaplin, Robert W Williams, John D Mountz

ABSTRACT

Interleukin 17 (IL-17) is a cytokine associated with inflammation, autoimmunity and defense against some bacteria. Here we show that IL-17 can promote autoimmune disease through a mechanism distinct from its proinflammatory effects. As compared with wild-type mice, autoimmune BXD2 mice express more IL-17 and show spontaneous development of germinal centers (GCs) before they increase production of pathogenic autoantibodies. We show that blocking IL-17 signaling disrupts CD4+ T cell and B cell interactions required for the formation of GCs and that mice lacking the IL-17 receptor have reduced GC B cell development and humoral responses. Production of IL-17 correlates with upregulated expression of the genes Rgs13 and Rgs16, which encode regulators of G-protein signaling, and results in suppression of the B cell chemotactic response to the chemokine CXCL12. These findings suggest a mechanism by which IL-17 drives autoimmune responses by promoting the formation of spontaneous GCs. More... »

PAGES

166-175

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni1552

DOI

http://dx.doi.org/10.1038/ni1552

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1038491172

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18157131


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26 schema:description Interleukin 17 (IL-17) is a cytokine associated with inflammation, autoimmunity and defense against some bacteria. Here we show that IL-17 can promote autoimmune disease through a mechanism distinct from its proinflammatory effects. As compared with wild-type mice, autoimmune BXD2 mice express more IL-17 and show spontaneous development of germinal centers (GCs) before they increase production of pathogenic autoantibodies. We show that blocking IL-17 signaling disrupts CD4+ T cell and B cell interactions required for the formation of GCs and that mice lacking the IL-17 receptor have reduced GC B cell development and humoral responses. Production of IL-17 correlates with upregulated expression of the genes Rgs13 and Rgs16, which encode regulators of G-protein signaling, and results in suppression of the B cell chemotactic response to the chemokine CXCL12. These findings suggest a mechanism by which IL-17 drives autoimmune responses by promoting the formation of spontaneous GCs.
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34 BXD2 mice
35 CD4
36 CXCL12
37 GC B cell development
38 IL-17
39 IL-17 correlates
40 IL-17 receptor
41 RGS13
42 RGS16
43 T helper cells
44 autoantibodies
45 autoimmune BXD2 mice
46 autoimmune diseases
47 autoimmune response
48 autoimmunity
49 autoreactive germinal center development
50 bacteria
51 cell chemotactic responses
52 cell development
53 cell interactions
54 cells
55 center
56 center development
57 chemokine CXCL12
58 chemotactic response
59 correlates
60 cytokines
61 defense
62 development
63 disease
64 disrupts CD4
65 effect
66 expression
67 findings
68 formation
69 formation of GCs
70 genes Rgs13
71 germinal center development
72 germinal centers
73 helper cells
74 humoral response
75 inflammation
76 interaction
77 interleukin 17
78 interleukin 17 orchestrate autoreactive germinal center development
79 interleukin 17-producing T helper cells
80 mechanism
81 mice
82 orchestrate autoreactive germinal center development
83 pathogenic autoantibodies
84 production
85 proinflammatory effects
86 protein signaling
87 receptors
88 regulator
89 response
90 results
91 signaling
92 spontaneous development
93 spontaneous germinal centers
94 suppression
95 upregulated expression
96 wild-type mice
97 schema:name Interleukin 17–producing T helper cells and interleukin 17 orchestrate autoreactive germinal center development in autoimmune BXD2 mice
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