Identification and Characterization of the Antigen Presenting Cell in Rat Autoimmune Myocarditis: Evidence of Bone Marrow Derivation and Non-requirement for MHC Class I Compatibility with Pathogenic T Cells

Ratcliffe, Nora R.; Wegmann, Keith W.; Zhao, Richard W; Hickey, William F.

doi:10.1006/jaut.2000.0431

Cited by 9 publications

(6 citation statements)

References 33 publications

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“…18,19 Interestingly, systemic activation of the innate immune system with TLR stimuli such as LPS results in upregulation of activation markers and myosin heavy chain class II molecules on heart-resident cells. 18 Furthermore, LPS injection results in relapses of inflammatory infiltrates and more rapid progression of heart failure in immunized mice.…”

Section: Discussionmentioning

confidence: 99%

“…16 During myocarditis development, recruitment of activated bone marrow-derived DCs precedes the accumulation of macrophages and T cells in the heart. [17][18][19] Accordingly, disease induction by adoptive transfer of heartspecific CD4 ϩ T cells requires pretreatment of recipient mice with lipopolysaccharide (LPS) and other strong TLR stimulants that upregulate myosin heavy chain class II expression on heart-resident DCs. 18 MyD88 is an essential adaptor molecule that mediates complex proinflammatory pathways that involve a cascade of kinases integrating both TLR4 and IL-1 receptor type 1 activation.…”

Section: Clinical Perspective P 265mentioning

confidence: 99%

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MyD88 Signaling Controls Autoimmune Myocarditis Induction

et al. 2006

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Background— Experimental autoimmune myocarditis (EAM) is a CD4 + T-cell–mediated mouse model of postviral cardiomyopathy. Activation of interleukin-1 type 1 and Toll-like receptors that share the common downstream adaptor molecule MyD88 is required for disease induction. The specific role of MyD88 in myocarditis, however, is not known. Methods and Results— In contrast to control littermates, MyD88 −/− mice were protected from myocarditis after immunization with α-myosin heavy chain–derived peptide (MyHC-α) and complete Freund’s adjuvant. Disease resistance of MyD88 −/− mice resulted from impaired expansion of heart-specific CD4 + T cells after immunization. Intrinsic defects of MyD88 −/− CD4 + T cells were excluded. In contrast, MyD88 −/− but not MyD88 +/+ primary antigen presenting dendritic cells (DCs) were defective in their capacity to prime CD4 + T cells. This defect mainly resulted from the inability of MyD88 −/− DCs to release tumor necrosis factor-α. The critical role of MyD88 signaling in DCs in the peripheral lymphatic compartments was finally proven by repetitive injection of activated, MyHC-α–loaded MyD88 +/+ DCs that fully restored T-cell expansion and myocarditis in MyD88 −/− mice. Conclusions— Autoimmune myocarditis induction depends on MyD88 signaling in self-antigen presenting cells in the peripheral compartments. We conclude that MyD88 might become a target for prevention of heart-specific autoimmunity and cardiomyopathy.

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Section: Discussionmentioning

confidence: 99%

Section: Clinical Perspective P 265mentioning

confidence: 99%

MyD88 Signaling Controls Autoimmune Myocarditis Induction

et al. 2006

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“…Interestingly, these cells constitutively express cardiac self-antigens on MHC class II molecules even in the healthy heart [18]. These cells accumulate during the development of heart-specific inflammation and up-regulate their MHC class II molecules in the presence of non-specific inflammatory stimulation [34][35][36]. So far, the role of these heart resident dendritic cells is not clear.…”

Section: Dendritic Cell Induced Autoimmune Heart Failurementioning

confidence: 99%

Dendritic cells and autoimmune heart failure

Marty

Eriksson

2006

International Journal of Cardiology

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“…In the EAM model, the development of inflammatory infiltrates depends on the sequential activation of self-antigen presenting DCs, the expansion of self-pathogenic T cells, and the accumulation of monocytes/ macrophages within the heart [33, [52][53][54][55]. DCs represent major of APCs representing scavengers for cellular debris and key players balancing the immune responses against foreign antigens and the maintenance of peripheral self-tolerance [56,57].…”

Section: Future Strategies: Targeting Innate Mechanisms Of Immune Actmentioning

confidence: 99%

Understanding the Cardiovascular Actions of Soy Isoflavones: Potential Novel Targets for Antihypertensive Drug Development

Martin¹,

Song²,

Mark³

et al. 2008

CHDDT

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Inflammatory cardiomyopathy is a common cause of heart failure developing on a basis of cardiac inflammation. Cardiac inflammation - or myocarditis - is usually triggered by infections or cardiac damage of any cause. Experimental autoimmune myocarditis refers to a CD4(+) T cell-mediated mouse model of inflammatory cardiomyopathy. So far, the experimental autoimmune myocarditis model helped us to understand the role of various chemokines, cytokines, and cell subsets in the progression of inflammatory heart disease. Here, we review the current therapeutic options for inflammatory cardiomyopathy, and delineate potential future treatment approaches from the most recent mechanistic insights given by the experimental autoimmune myocarditis model.

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Identification and Characterization of the Antigen Presenting Cell in Rat Autoimmune Myocarditis: Evidence of Bone Marrow Derivation and Non-requirement for MHC Class I Compatibility with Pathogenic T Cells

Cited by 9 publications

References 33 publications

MyD88 Signaling Controls Autoimmune Myocarditis Induction

MyD88 Signaling Controls Autoimmune Myocarditis Induction

Dendritic cells and autoimmune heart failure

Understanding the Cardiovascular Actions of Soy Isoflavones: Potential Novel Targets for Antihypertensive Drug Development

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