IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-β

Ines Gonzalez-García; Yani Zhao; Songguang Ju; Qin Gu; Lin Liu; Jay K. Kolls; Binfeng Lu

doi:10.4049/jimmunol.0802221

IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-β

Ines Gonzalez-García
, Yani Zhao
, Songguang Ju
, Qin Gu
, Lin Liu
, Jay K. Kolls
, Binfeng Lu

Center for Discovery and Innovation

University of Pittsburgh

Research output: Contribution to journal › Article › peer-review

36 Scopus citations

Abstract

Recent studies have established an important role of Th17 in induction of autoimmune diseases. We have found that although IL-17 receptor A (IL-17RA) ^-/- mice were resistant to experimental autoimmune encephalomyelitis, a small number of them developed milder clinical signs of this autoimmune disease. In addition, blockade of TGF-β in IL-17RA^-/- mice resulted in much more severe clinical signs of experimental autoimmune encephalomyelitis and significantly increased parenchymal lymphocyte infiltration in the CNS. Furthermore, the number of autoreactive Th1 cells was greatly increased in the inflamed spinal cord of IL-17RA^-/- mice. These data support a role of IL-17RA-independent mechanisms in causing autoimmunity and its regulation by TGF-β.

Original language	English
Pages (from-to)	2665-2671
Number of pages	7
Journal	Journal of Immunology
Volume	182
Issue number	5
DOIs	https://doi.org/10.4049/jimmunol.0802221
State	Published - 1 Mar 2009

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title = "IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-β",

abstract = "Recent studies have established an important role of Th17 in induction of autoimmune diseases. We have found that although IL-17 receptor A (IL-17RA) -/- mice were resistant to experimental autoimmune encephalomyelitis, a small number of them developed milder clinical signs of this autoimmune disease. In addition, blockade of TGF-β in IL-17RA-/- mice resulted in much more severe clinical signs of experimental autoimmune encephalomyelitis and significantly increased parenchymal lymphocyte infiltration in the CNS. Furthermore, the number of autoreactive Th1 cells was greatly increased in the inflamed spinal cord of IL-17RA-/- mice. These data support a role of IL-17RA-independent mechanisms in causing autoimmunity and its regulation by TGF-β.",

author = "Ines Gonzalez-Garc{\'i}a and Yani Zhao and Songguang Ju and Qin Gu and Lin Liu and Kolls, \{Jay K.\} and Binfeng Lu",

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T1 - IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-β

AU - Gonzalez-García, Ines

AU - Zhao, Yani

AU - Ju, Songguang

AU - Gu, Qin

AU - Liu, Lin

AU - Kolls, Jay K.

AU - Lu, Binfeng

PY - 2009/3/1

Y1 - 2009/3/1

N2 - Recent studies have established an important role of Th17 in induction of autoimmune diseases. We have found that although IL-17 receptor A (IL-17RA) -/- mice were resistant to experimental autoimmune encephalomyelitis, a small number of them developed milder clinical signs of this autoimmune disease. In addition, blockade of TGF-β in IL-17RA-/- mice resulted in much more severe clinical signs of experimental autoimmune encephalomyelitis and significantly increased parenchymal lymphocyte infiltration in the CNS. Furthermore, the number of autoreactive Th1 cells was greatly increased in the inflamed spinal cord of IL-17RA-/- mice. These data support a role of IL-17RA-independent mechanisms in causing autoimmunity and its regulation by TGF-β.

AB - Recent studies have established an important role of Th17 in induction of autoimmune diseases. We have found that although IL-17 receptor A (IL-17RA) -/- mice were resistant to experimental autoimmune encephalomyelitis, a small number of them developed milder clinical signs of this autoimmune disease. In addition, blockade of TGF-β in IL-17RA-/- mice resulted in much more severe clinical signs of experimental autoimmune encephalomyelitis and significantly increased parenchymal lymphocyte infiltration in the CNS. Furthermore, the number of autoreactive Th1 cells was greatly increased in the inflamed spinal cord of IL-17RA-/- mice. These data support a role of IL-17RA-independent mechanisms in causing autoimmunity and its regulation by TGF-β.

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DO - 10.4049/jimmunol.0802221

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AN - SCOPUS:64849085127

SN - 0022-1767

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SP - 2665

EP - 2671

JO - Journal of Immunology

JF - Journal of Immunology

IS - 5

ER -

IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-β

Abstract

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