STAT4 controls GM-CSF production by both Th1 and Th17 cells during EAE.

ABSTRACT:

Background

In experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, mice genetically deficient in the transcription factor signal transducer and activator of transcription 4 (STAT4) are resistant to disease. In contrast, deletion or inhibition of the Th1-associated cytokines IL-12 or IFNγ which act upstream and downstream of STAT4, respectively, does not ameliorate disease. These discordant findings imply that STAT4 may act in a non-canonical role during EAE. Recently, STAT4 has been shown to regulate GM-CSF production by CD4 T cells and this cytokine is necessary for the induction of EAE. However, it is not known if STAT4 controls GM-CSF production by both Th1 and Th17 effector CD4 T cells.

Methods

This study utilized the MOG(35-55) peptide i

SUBMITTER: McWilliams IL 

PROVIDER: S-EPMC4491892 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature