PMID- 23181351 OWN - NLM STAT- MEDLINE DCOM- 20130426 LR - 20211021 IS - 1365-2567 (Electronic) IS - 0019-2805 (Print) IS - 0019-2805 (Linking) VI - 138 IP - 4 DP - 2013 Apr TI - All-trans-retinoic acid ameliorates experimental allergic encephalomyelitis by affecting dendritic cell and monocyte development. PG - 333-45 LID - 10.1111/imm.12040 [doi] AB - Experimental allergic encephalomyelitis (EAE) can be induced in animal models by injecting the MOG35-55 peptide subcutaneously. Dendritic cells (DCs) that are located at the immunization site phagocytose the MOG35-55 peptide. These DCs mature and migrate into the nearest draining lymph nodes (dLNs), then present antigen, resulting in the activation of naive T cells. T helper type 1 (Th1) and Th17 cells are the primary cells involved in EAE progression. All-trans-retinoic acid (AT-RA) has been shown to have beneficial effects on EAE progression; however, whether AT-RA influences DC maturation or mediates other functions is unclear. In the present study, we showed that AT-RA led to the down-regulation of MHC class II, CD80 (B7-1) and CD86 (B7-2) expressed on the surface of DCs that were isolated from dLNs or spleen 3 days post-immunization in an EAE model. Changes to DC function influenced Th1/Th17 subset polarization. Furthermore, the number of CD44(+) monocytes (which might trigger EAE progression) was also significantly decreased in dLNs, spleen, subarachnoid space and the spinal cord parenchyma after AT-RA treatment. These findings are the first to demonstrate that AT-RA impairs the antigen-presenting capacity of DCs, leading to down-regulation of pathogenic Th1 and Th17 inflammatory cell responses and reducing EAE severity. CI - (c) 2012 Blackwell Publishing Ltd. FAU - Zhan, Xiao-Xia AU - Zhan XX AD - Department of Neurobiology, Harbin Medical University Provincial Key Laboratory of Neurobiology, Harbin Medical University, Harbin, Heilongjiang, China. FAU - Liu, Yu AU - Liu Y FAU - Yang, Jin-Feng AU - Yang JF FAU - Wang, Guang-You AU - Wang GY FAU - Mu, Lili AU - Mu L FAU - Zhang, Tong-Shuai AU - Zhang TS FAU - Xie, Xiao-Li AU - Xie XL FAU - Wang, Jing-Hua AU - Wang JH FAU - Liu, Yu-Mei AU - Liu YM FAU - Kong, Qing-Fei AU - Kong QF FAU - Li, Hu-Lun AU - Li HL FAU - Sun, Bo AU - Sun B LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Immunology JT - Immunology JID - 0374672 RN - 0 (Antigens, CD) RN - 0 (Antioxidants) RN - 0 (Histocompatibility Antigens Class II) RN - 0 (Myelin-Oligodendrocyte Glycoprotein) RN - 0 (Peptide Fragments) RN - 0 (myelin oligodendrocyte glycoprotein (35-55)) RN - 5688UTC01R (Tretinoin) SB - IM MH - Animals MH - Antigen Presentation/drug effects MH - Antigens, CD/genetics/immunology MH - Antioxidants/pharmacology/*therapeutic use MH - Cell Differentiation/drug effects MH - Dendritic Cells/*drug effects/immunology/pathology MH - Encephalomyelitis, Autoimmune, Experimental/chemically induced/*drug therapy/immunology/pathology MH - Female MH - Gene Expression Regulation/drug effects MH - Histocompatibility Antigens Class II/genetics/immunology MH - Immunization MH - Lymph Nodes/drug effects/immunology/pathology MH - Mice MH - Mice, Inbred C57BL MH - Monocytes/*drug effects/immunology/pathology MH - Myelin-Oligodendrocyte Glycoprotein MH - Peptide Fragments MH - Signal Transduction/drug effects MH - Spinal Cord/drug effects/immunology/pathology MH - Spleen/drug effects/immunology/pathology MH - Th1 Cells/drug effects/immunology/pathology MH - Th17 Cells/drug effects/immunology/pathology MH - Tretinoin/pharmacology/*therapeutic use PMC - PMC3719944 EDAT- 2012/11/28 06:00 MHDA- 2013/04/27 06:00 PMCR- 2014/04/01 CRDT- 2012/11/28 06:00 PHST- 2012/04/16 00:00 [received] PHST- 2012/11/15 00:00 [revised] PHST- 2012/11/16 00:00 [accepted] PHST- 2012/11/28 06:00 [entrez] PHST- 2012/11/28 06:00 [pubmed] PHST- 2013/04/27 06:00 [medline] PHST- 2014/04/01 00:00 [pmc-release] AID - 10.1111/imm.12040 [doi] PST - ppublish SO - Immunology. 2013 Apr;138(4):333-45. doi: 10.1111/imm.12040.