Abstract:
:MS and EAE are T cell-driven autoimmune diseases of the CNS where IL-17-producing Th17 cells promote damage and are pathogenic. Conversely, tolerogenic DCs induce Treg cells and suppress Th17 cells. Chloroquine (CQ) suppresses EAE through the modulation of DCs by unknown mechanisms. Here, we show that STAT 1 is necessary for CQ-induced tolerogenic DCs (tolDCs) to efficiently suppress EAE. We observed that CQ induces phosphorylation of STAT1 in DCs in vivo and in vitro. Genetic blockage of STAT1 abrogated the suppressive activity of CQ-treated DCs. Opposed to its WT counterparts, CQ-treated STAT1-/- BMDCs were unable to suppress Th17 cells and increased EAE severity. Our findings show that STAT1 is a major signaling pathway in CQ-induced tolDCs and may shed light on new therapeutic avenues for the induction of tolDCs in autoimmune diseases such as MS.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Thome R,Bonfanti AP,Rasouli J,Mari ER,Zhang GX,Rostami A,Verinaud Ldoi
10.1002/eji.201747362subject
Has Abstractpub_date
2018-07-01 00:00:00pages
1228-1234issue
7eissn
0014-2980issn
1521-4141journal_volume
48pub_type
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