IL-17 Signaling-Independent Central Nervous System Autoimmunity Is Negatively Regulated by TGF-β | Zendy

Inés González-Garcı́a | Zendy; Yani Zhao | Zendy; Songguang Ju | Zendy; Qin Gu | Zendy; Lin Liu | Zendy; Jay K. Kolls | Zendy; Binfeng Lu | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

IL-17 Signaling-Independent Central Nervous System Autoimmunity Is Negatively Regulated by TGF-β

Author(s) -

Inés González-Garcı́a,

Yani Zhao,

Songguang Ju,

Qin Gu,

Lin Liu,

Jay K. Kolls,

Binfeng Lu

Publication year - 2009

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.0802221

Subject(s) - experimental autoimmune encephalomyelitis , autoimmunity , immunology , autoimmune disease , central nervous system , medicine , interleukin 17 , transforming growth factor , receptor , cytokine , multiple sclerosis , immune system , endocrinology , antibody

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-beta 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-beta.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research