JCI - Coaxing the liver into preventing autoimmune disease in the brain

Coaxing the liver into preventing autoimmune disease in the brain

Brad E. Hoffman, Roland W. Herzog

Published in Volume 118, Issue 10

J Clin Invest. 2008; 118(10):3271–3273 doi:10.1172/JCI37079

Abstract | Full text | PDF

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Figure 1

Prevention of EAE in mice by hepatic expression of MBP.

(A) Immunization with MBP-specific peptide normally causes an inflammatory T cell response in the brain in the EAE mouse model of human MS. (B) In the study by Lüth et al. in this issue of the JCI (20), the authors show that hepatic expression of MBP (normally expressed in the central nervous system), accomplished constitutively in liver-specific MBP transgenic mice (not shown) or transiently after gene transfer to liver cells in vivo, results in induction of MBP-specific CD4⁺CD25⁺Foxp3⁺ Tregs. These MBP-specific CD4⁺CD25⁺Foxp3⁺ Tregs suppressed effector CD4⁺CD25^– T cells and converted conventional CD4⁺CD25^– T cells into CD4⁺CD25⁺Foxp3⁺ Tregs, thereby preventing neuroinflammatory disease. Introduction of antigens to the liver may have potential as a preventative or therapeutic intervention for autoimmune disease.