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Innate Signaling Promotes Formation of Regulatory Nitric Oxide–Producing Dendritic Cells Limiting T-Cell Expansion in Experimental Autoimmune...
Update time:2016-09-25 23:28:00   【 Font: Large  Medium Small

Innate Signaling Promotes Formation of Regulatory Nitric Oxide–Producing Dendritic Cells Limiting T-Cell Expansion in Experimental Autoimmune Myocarditis


Background—Activation of innate pattern-recognition receptors promotes CD4+ T-cell–mediated autoimmune myocarditis and subsequent inflammatory cardiomyopathy. Mechanisms that counterregulate exaggerated heart-specific autoimmunity are poorly understood.

Methods and Results—Experimental autoimmune myocarditis was induced in BALB/c mice by immunization with α-myosin heavy chain peptide and complete Freund’s adjuvant. Together with interferon-γ, heat-killedMycobacterium tuberculosis, an essential component of complete Freund’s adjuvant, converted CD11bhiCD11c monocytes into tumor necrosis factor-α– and nitric oxide synthase 2–producing dendritic cells (TipDCs). Heat-killed M. tuberculosis stimulated production of nitric oxide synthase 2 via Toll-like receptor 2–mediated nuclear factor-κB activation. TipDCs limited antigen-specific T-cell expansion through nitric oxide synthase 2–dependent nitric oxide production. Moreover, they promoted nitric oxide synthase 2 production in hematopoietic and stromal cells in a paracrine manner. Consequently, nitric oxide synthase 2 production by both radiosensitive hematopoietic and radioresistant stromal cells prevented exacerbation of autoimmune myocarditis in vivo.

Conclusions—Innate Toll-like receptor 2 stimulation promotes formation of regulatory TipDCs, which confine autoreactive T-cell responses in experimental autoimmune myocarditis via nitric oxide. Therefore, activation of innate pattern-recognition receptors is critical not only for disease induction but also for counterregulatory mechanisms, protecting the heart from exaggerated autoimmunity.

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Source:Circulation      by Kania G, Siegert S, Behnke S, et al.
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