Stay Connected. Manage Your Care.
Access your health information anytime and anywhere, at home or on the go, with MyHealth.
- Message your clinic
- View your lab results
- Schedule your next appointment
- Pay your bill
The MyHealth mobile app from Stanford Health Care puts all your health information at your fingertips and makes managing your health care simple and quick.
Guest Services
24/7
We are available to assist you
whenever you need it. Give us a call at
650-498-3333 or
PHYSICIAN HELPLINE
Have a question? We're here to help! Call 1-866-742-4811
Monday - Friday, 8 a.m. - 5 p.m.
REFER A PATIENT
Fax 650-320-9443
Track your patients' progress and communicate with Stanford providers conveniently and securely.
Abstract
Autoimmune encephalomyelitis, a mouse model for multiple sclerosis, is characterized by the activation of immune cells, demyelination of axons in the CNS, and paralysis. We found that TGF-beta1 synthesis in glial cells and TGF-beta-induced signaling in the CNS were activated several days before the onset of paralysis in mice with autoimmune encephalomyelitis. While early production of TGF-beta1 was observed in glial cells TGF-beta signaling was activated in neurons and later in infiltrating T cells in inflammatory lesions. Systemic treatment with a pharmacological inhibitor of TGF-beta signaling ameliorated the paralytic disease and reduced the accumulation of pathogenic T cells and expression of IL-6 in the CNS. Priming of peripheral T cells was not altered, nor was the generation of TH17 cells, indicating that this effect was directed within the brain, yet affected the immune system. These results suggest that early production of TGF-beta1 in the CNS creates a permissive and dangerous environment for the initiation of autoimmune inflammation, providing a rare example of the brain modulating the immune system. Importantly, inhibition of TGF-beta signaling may have benefits in the treatment of the acute phase of autoimmune CNS inflammation.
View details for DOI 10.1172/JCI31763
View details for Web of Science ID 000250676000023
View details for PubMedID 17965773