What question did this study set out to answer?

To determine the mechanistic role of interleukin-10 (IL-10) in the induction of nasal tolerance and the regulation of autoimmune myocarditis.

February 1, 2002The Journal of ImmunologyOpen Access

Cutting Edge: A Critical Role for IL-10 in Induction of Nasal Tolerance in Experimental Autoimmune Myocarditis

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Why the study?

Does IL-10 play a critical role in the induction of nasal tolerance and suppression of experimental autoimmune myocarditis?

Population

Experimental autoimmune myocarditis model

Design

Preclinical

Authors

ZKZiya KayaInterventional Cardiology KDKazufumi DohmenFukuoka Hospital YWYan WangShriners Hospitals for Children - Erie

Discussion

Member takes

Implication

IL-10 dependence of nasal tolerance in myocarditis models; extends preclinical mechanisms but leaves open human translation.

Key Points

To determine the mechanistic role of interleukin-10 (IL-10) in the induction of nasal tolerance and the regulation of autoimmune myocarditis.
Induced experimental autoimmune myocarditis and administered cardiac antigen intranasally to establish mucosal tolerance.
Neutralized IL-10 during nasal tolerization, the induction phase, or the effector phase to evaluate changes in disease severity, antibody titers, and cytokine profiles.
Blocking IL-10 concurrently with nasal antigen administration abolished disease suppression and increased cardiac myosin-specific IL-1 and TNF-alpha production.
Blocking IL-10 during the effector phase increased disease incidence, severity, antigen-specific IL-2, IL-4, and TNF-alpha, and cardiac myosin-specific IgG1 and IgG2b, whereas blockade during the induction phase had no effect.

Structured PICO

Does IL-10 play a critical role in the induction of nasal tolerance and suppression of experimental autoimmune myocarditis?

Population

Experimental autoimmune myocarditis model

Intervention

Blocking IL-10 (concurrent with nasal administration of antigen, during the effector phase, or during the induction phase)

Outcome

Incidence and severity of disease, and antigen-specific cytokine (IL-1, IL-2, IL-4, TNF-alpha) and antibody (IgG1, IgG2b) productionsurrogate

IL-10 is critical for the induction of nasal tolerance and limits inflammation during the effector phase of experimental autoimmune myocarditis.

Cite This Study

Kaya et al. (2002) studied this question.

synapsesocial.com/papers/6a73c212d0d1650e4d69f1c2 https://doi.org/10.4049/jimmunol.168.4.1552

Topics

Myocarditis

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Cutting Edge: A Critical Role for IL-10 in Induction of Nasal Tolerance in Experimental Autoimmune Myocarditis

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Cutting Edge: A Critical Role for IL-10 in Induction of Nasal Tolerance in Experimental Autoimmune Myocarditis

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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