Acute pericarditis in the post-myocardial infarction patient

Turk, Michelle L.

doi:10.1097/00002727-198912000-00005

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“…Clinical studies report occurrence of post myocardial infarction pericarditis in a relevant proportion of patients (71–78). However, molecular pathomechanisms of the infarction-related myocarditis syndrome remained unclear.…”

Section: Discussionmentioning

confidence: 99%

The Proteoglycan Biglycan Enhances Antigen-Specific T Cell Activation Potentially via MyD88 and TRIF Pathways and Triggers Autoimmune Perimyocarditis

Popović

Wang

Papatriantafyllou

et al. 2011

The Journal of Immunology

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Biglycan is a proteoglycan ubiquitously present in extracellular matrix of a variety of organs including heart and has been reported to be overexpressed in myocardial infarction. Myocardial infarction may be complicated by perimyocarditis through to date unclear mechanisms. Our aim was to investigate the capacity of TLR2/TLR4 ligand biglycan to enhance the presentation of specific Ags released upon cardiomyocyte necrosis. In vitro, Ova-pulsed bone-marrow derived dendritic cells from WT (C57BL/6), TLR2-, TLR4-, MyD88- or TRIF- deficient mice were co-treated with LPS, biglycan or vehicle and incubated with Ova-recognizing MHCI- or MHCII-restricted T cells. Biglycan enhanced Ova-specific cross-priming by more than 80% to MHCI-restricted T cells in both TLR2 - and TLR4 – pathway dependent manner. Accordingly, biglycan-induced cross-priming by both MyD88- and TRIF-deficient DCs was strongly diminished. Ova-specific activation of MHCII-restricted T cells was predominantly TLR4-dependent. Our first in vivo correlate was a model of experimental autoimmune perimyocarditis triggered by injection of cardiac-Ag pulsed DCs (BALB/c). Biglycan-treated DCs triggered perimyocarditis in extent and intensity comparable to LPS-treated DCs (average scores 1.3±0.3 and 1.5±0.4, respectively). Substitution with TLR4-deficient DCs abolished this effect. In a second in vivo approach, WT and biglycan-deficient mice were followed two weeks after induction of myocardial infarction. WT mice demonstrated significantly higher myocardial T-lymphocyte infiltration in comparison to biglycan-deficient animals. We conclude that TLR2/4 ligand biglycan, a component of the myocardial matrix, may enhance Ag-specific T cell priming via MyD88 and TRIF and stimulate autoimmune perimyocarditis.

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Section: Discussionmentioning

confidence: 99%