The genome organizer special AT-rich sequence binding protein 1 (SATB1) 
regulates specific functions through chromatin remodeling in T helper cells. It 
was recently reported by our team that T cells from SATB1 conditional knockout 
(SATB1cKO) mice, in which the Satb1 gene is deleted from hematopoietic cells, 
impair phosphorylation of signaling molecules in response to T cell receptor 
(TCR) crosslinking. However, in vivo T cell responses upon antigen presentation 
in the absence of SATB1 remain unclear. In the current study, it was shown that 
SATB1 modulates T cell antigen responses during the induction and effector 
phases. Expression of SATB1 was upregulated in response to TCR stimulation, 
suggesting that SATB1 is important for this antigen response. The role of SATB1 
in TCR responses and induced experimental autoimmune encephalomyelitis (EAE) was 
therefore examined using the myelin oligodendrocyte glycoprotein peptide 35-55 
(MOG35-55) and pertussis toxin. SATB1cKO mice were found to be resistant to EAE 
and had defects in IL-17- and IFN-γ-producing pathogenic T cells. Thus, SATB1 
expression appears necessary for T cell function in the induction phase. To 
examine SATB1 function during the effector phase, a tamoxifen-inducible SATB1 
deletion system, SATB1cKO-ER-Cre mice, was used. Encephalitogenic T cells from 
MOG35-55-immunized SATB1cKO-ER-Cre mice were transferred into healthy mice. Mice 
that received tamoxifen before the onset of paralysis were resistant to EAE. 
Furthermore, no disease progression occurred in recipient mice treated with 
tamoxifen after the onset of EAE. Thus, SATB1 is essential for maintaining TCR 
responsiveness during the induction and effector phases and may provide a novel 
therapeutic target for T cell-mediated autoimmune diseases.