10.3389/fimmu.2018.02714.s002 Katrien Van der Borght Katrien Van der Borght Charlotte L. Scott Charlotte L. Scott Liesbet Martens Liesbet Martens Dorine Sichien Dorine Sichien Gert Van Isterdael Gert Van Isterdael Veronika Nindl Veronika Nindl Yvan Saeys Yvan Saeys Louis Boon Louis Boon Burkhard Ludewig Burkhard Ludewig Thierry C. Gillebert Thierry C. Gillebert Bart N. Lambrecht Bart N. Lambrecht Data_Sheet_2_Myocarditis Elicits Dendritic Cell and Monocyte Infiltration in the Heart and Self-Antigen Presentation by Conventional Type 2 Dendritic Cells.PDF Frontiers 2018 dendritic cells myocarditis autoimmunity heart failure autoreactive T cells 2018-11-21 04:12:38 Dataset https://frontiersin.figshare.com/articles/dataset/Data_Sheet_2_Myocarditis_Elicits_Dendritic_Cell_and_Monocyte_Infiltration_in_the_Heart_and_Self-Antigen_Presentation_by_Conventional_Type_2_Dendritic_Cells_PDF/7368659 <p>Autoimmune myocarditis often leads to dilated cardiomyopathy (DCM). Although T cell reactivity to cardiac self-antigen is common in the disease, it is unknown which antigen presenting cell (APC) triggers autoimmunity. Experimental autoimmune myocarditis (EAM) was induced by immunizing mice with α-myosin loaded bone marrow APCs cultured in GM-CSF. APCs found in such cultures include conventional type 2 CD11b<sup>+</sup> cDCs (GM-cDC2s) and monocyte-derived cells (GM-MCs). However, only α-myosin loaded GM-cDC2s could induce EAM. We also studied antigen presenting capacity of endogenous type 1 CD24<sup>+</sup> cDCs (cDC1s), cDC2s, and MCs for α-myosin-specific TCR-transgenic TCR-M CD4<sup>+</sup> T cells. After EAM induction, all cardiac APCs significantly increased and cDCs migrated to the heart-draining mediastinal lymph node (LN). Primarily cDC2s presented α-myosin to TCR-M cells and induced Th1/Th17 differentiation. Loss of IRF4 in Irf4<sup>fl/fl</sup>.Cd11cCre mice reduced MHCII expression on GM-cDC2s in vitro and cDC2 migration in vivo. However, partly defective cDC2 functions in Irf4<sup>fl/fl</sup>.Cd11cCre mice did not suppress EAM. MCs were the largest APC subset in the inflamed heart and produced pro-inflammatory cytokines. Targeting APC populations could be exploited in the design of new therapies for cardiac autoimmunity.</p>