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Grant Recipients and their Research

Each year, the Myocarditis Foundation awards a research grant to fund the advancement of myocarditis understanding. Read about some of our past grant recipients and learn about the research our grant program helped fund.

2016 MF Fellowship Research Grant Recipient-Dr. Guobao Chen

The Myocarditis Foundation is pleased to announce that Dr. Guobao Chen, PhD, is the 2016 Fellowship Grant Recipient for the 2107-2018 Academic Year. Dr. Chen was the second place finalist in last year’s Fellowship Grant applicants, but came in above all the others in the 2016 submissions.Dr. Chen is from Johns Hopkins University School of Medicine and his mentor is Dr. Daniela Cihakova MD, PhD. Dr. Cihakova was the very first MF Fellowship Grant recipient in 2006. Dr. Chen is now conducting myocarditis research in Dr. Cihakova’s Lab and his research submission is entitled: “The Role of PDGFRa+ Cardiac Fibroblast in Myocarditis.”

Dr. Chen’s layman’s summary of his research project is as follows:

Despite that most patients recover from acute myocarditis, an estimated 9-16% of myocarditis cases progress to dilated cardiomyopathy, which is one of the most common causes of non-congenital heart failure in young individuals. Effective treatments for chronic dilated cardiomyopathy patients are limited, leaving heart transplantation as the only option for end stage heart failure. Thus, to stop the disease progression from myocarditis to dilated cardiomyopathy is critical for patients to recover from myocarditis.

We have adapted an experimental auto-immune myocarditis mouse model, to investigate the mechanism behind the disease progression from myocarditis to dilated cardiomyopathy. We have found a specific group of heart cells that is receiving the signaling from a pathological factor IL-17A. After receiving the signal from IL-17A, these cells will produce a number of other pathological factors to exacerbate the disease progression from myocarditis to dilated cardiomyopathy. We have also detected the same group of heart cells in human myocarditis patients and they were found to be expressing the pathological factors that were found in our mouse model. Similarly, the same specific group was also found in ischemia patient biopsies and our myocardial infarction (Heart Attack) mouse model. Thus, our discovery provides an excellent opportunity to develop specific treatment to halt the disease progression from myocarditis to dilated cardiomyopathy. We have designed delicate therapeutic methods to specifically target the immune function of this group of cells without killing them, which will minimize the side effects of systemic immune suppression and preserve other functions of these cells that might be important for the recovery from myocarditis.

A short story about how Dr. Chen joined Dr. Cihakova’s Lab at Johns Hopkins:

As previously an immunologist, I was first attracted by the sophisticated immune interactions between different cell types in the heart that were previously published by members of Dr. Cihakova’s Lab. From there, I went on to read more about myocarditis and diseases involving heart inflammation. It was after that when I became more and more interested with this topic. Later, in a routine conversation with my mum, she told me that her doctor suspected that she might have had myocarditis before, as her left ventricle was abnormally large. All these things strengthened my decision to dedicate my research career on developing treatment for myocarditis and other heart diseases.

The Myocarditis Foundation extends their best wishes to Dr. Chen for much success in his myocarditis research.  It is our prayer that we will one day find a treatment or a cure for this devastating disease, that takes so many of our young and otherwise healthy children and young adults.


The Myocarditis Foundation Welcomes Previous Fellowship Grant Recipient to the Medical Advisory Board!

Dr. Bettina Heidecker, the 2007 Myocarditis Foundation Fellowship Grant recipient, has just been appointed to the Myocarditis Foundation Medical Advisory Board. Dr. Heideckers title of her research at that time was: Gene Expression Profiling for Detection of Myocarditis.

Since that time, Dr. Heidecker, has worked with Dr. Joshua Hare at the University of Miami Interdisciplinary Stem Cell Institute as a Post-Doctoral Fellow and Co-Principal Investigator, (2007-2009) studying transcriptomic biomarkers for new onset heart failure and to further develop the diagnostic biomarker for myocarditis.

Dr. Heidecker also completed her residency training at the University of Miami in Internal Medicine (2009-2012) as well as a Cardiology fellowship at the University of California, San Francisco (2012-2015) while continuing her research in myocarditis.MF BETTINA H picture

Dr. Heidecker served as a member of the Scientific Advisory Board of Heart Genomics, LLC, a company that her preceptor, Dr. Joshua Hare founded. Her goal is to develop improved diagnostic accuracy in myocarditis by analyzing heart biopsies and blood samples of patients with myocarditis and to get a better understanding of the pathophysiology of this common disease She has also been an International Lecturer in Cardiology for the Aston Medical School in Birmingham, UK since 2014.

Dr. Heidecker has returned to her homeland of Austria in September 2015 and is now a non-invasive cardiologist at the University of Zurich, Switzerland, where she teaches students and fellows early recognition of myocarditis. Furthermore, she established a specialty clinic for myocarditis and is planning to start enrolling patients soon for at least two clinical studies in the field of myocarditis.

Her professional memberships include:
European Society of Cardiology: Working Group on Myocardial and Pericardial Diseases
European Acute Cardiovascular Care Association
American College of Cardiology
American Heart Association
American Society of Echocardiography
sterreichische Gesellschaft fr Innere Medizin

Dr. Heidecker has had many published articles in her field of research and has always been a supporter of the Myocarditis Foundation. She expressed in a 2015 European Heart Journal article that the Myocarditis Foundation was especially helpful for her, through its financial support and the mentorship of Drs. Leslie Cooper and DeLisa Fairweather.

We look forward to our continued association with her and utilizing her impressive achievements to help direct our future research initiatives.

Welcome Dr. Heidecker!


The Myocarditis Foundation Announces its 2015 Grant Recipient for the 2016/2017 Grant Cycle

The Myocarditis Foundation is pleased to announce that it will be funding a research fellowship grant for the 2016/2017 grant cycle. The Myocarditis Foundation will be awarding the research grant to Dr. Jon Sin of Cedars-Sinai Medical Center in the amount of $40,000. Dr. Sin is under the mentorship of Dr. Ralph Feuer of Cedars-Sinai Medical Center.

Jon Sin

The Myocarditis Foundation, an international non-profit organization founded in 2005, is dedicated to increasing awareness and hastening progress in understanding this rare disease. Myocarditis is a disease that is marked by inflammation and scarring of the heart muscle, which can progress rapidly to heart failure and death or heart transplantation.

The Myocarditis Foundation announced in its third quarter of 2015 that it was accepting grant applications until December 1, 2015. The Myocarditis Foundations International Medical Advisory Board, made up of leading myocarditis researchers from around the world, voted to award a fellowship grant to Dr. Sin after selecting his application from a distinguished field of candidates.

Dr. Sins research project is titled Coxsackievirus B Subverts Host Mitophagy to Promote Viral Dissemination and Myocarditis. Below is a laymans summary of his research:

Coxsackievirus B (CVB) is a common juvenile pathogen that can cause a wide-array of inflammatory diseases including meningitis, pancreatitis, and myocarditis, all of which can be fatal. We see that CVB, which is a naked virus, can escape the cell in membrane-bound vesicles which we hypothesize are derived from autophagosomes. Not only does this blur the line between enveloped and non-enveloped viruses, but it also suggests that CVB could use these host membranes to evade the immune system. Additionally when we infect cardiomyocytes, mitochondrial networks appear to fragment, which is an early step in the autophagic degradation of mitochondria (mitophagy). Normally, these fragmented mitochondria would be targeted for destruction; however we find that in the setting of infection, mitochondrial fragments and virus are ejected from the cell in membrane-bound vesicles. If we pharmacologically block mitochondrial fission prior to infection, this results in lower viral titers in the media and fewer infected cells, suggesting that blocking the early steps in mitophagy suppresses viral escape. We hypothesize that the virus triggers mitochondrial fission and uses these fragments as bait in order to become encapsulated in autophagosomes and get ejected from the cell in order to further spread infection. Based on our preliminary findings, we are now utilizing a mouse model of CVB infection to test the efficacy of using a mitochondrial fission inhibitor to suppress vital myocarditis.

-Summary by Dr. Sin

The Myocarditis Foundation is honored to work with Dr. Sin and the Cedars-Sinai Medical Center, furthering the expansion of myocarditis research. It is the Foundations goal to build a greater understanding of the disease and find better ways to diagnose, treat and ultimately prevent myocarditis from taking more lives.

The Myocarditis Foundation would like to thank all the families, businesses, and organizations that have supported the Foundation in 2015. It is with their generosity and support that these research grants are able to be awarded each year.

For more information regarding the Myocarditis Foundation and its grant program, please visit, www.myocarditisfoundation.org.


Success in Mentoring MF Grant Recipient

The Myocarditis Foundation awards grants for one year research fellowships to study myocarditis with the aim of encouraging young PhD and MD scientists to pursue a career involving myocarditis. As well as financial support the Foundation also provides mentoring support with career advice and assistance with networking. Recently one of our grant recipients, Dr. Bettina Heidecker MD, was highlighted in an article in a prestigious scientific journal the European Heart Journal (reference Eur Heart J (2015) 36:398-403). In this article Bettina states that Myocarditis is a disease affecting many young individuals. Currently we lack sufficient understanding of its pathophysiology to improve specific treatment. With current standard diagnostic techniques a large number of patients with myocarditis remain under-diagnosed and therefore do not receive appropriate treatment. Bettinas research received funding support not only from the Myocarditis Foundation but also from the American Heart Association. She received a Samuel A. Levine Award and a Jay N. Cohn New Investigator Award based on her research findings. She mentions in her article how important funding from the MF and mentoring from Dr. Leslie Cooper MD and Dr. DeLisa Fairweather PhD, MF Board Members, was for her career success. She currently is a Cardiology Fellow at UCSF and plans to combine research, clinical work, and teaching in her career. MF grant recipients who have become Assistant Professors in Faculty positions include Dr. Daniela Cihakova MD, PhD at Johns Hopkins School of Medicine and Dr. David Marchant, PhD at the University of Alberta Canada. We are proud of the success of all of our grant recipients.


The Myocarditis Foundation Announces its 2014 Grant Recipient for the 2015/16 Grant Cycle

The Myocarditis Foundation is pleased to announce that it will be funding a research fellowship grant for the 2015/16 grant cycle. The Myocarditis Foundation will be funding a research grant awarded to Dr. Michael Bode of the University of North Carolina in the amount of $35,000. Dr. Bode is under the mentorship of Dr. Nigel Mackman of the University of North Carolina.

Michael Bod

The Myocarditis Foundation, an international non-profit organization founded in 2005, is dedicated to increasing awareness and hastening progress in understanding this rare disease. Myocarditis is a disease that is marked by inflammation and scarring of the heart muscle, which can progress rapidly to heart failure and death or heart transplantation.

The Myocarditis Foundation announced in its third quarter of 2014 that it was accepting grant applications until December 2014. The Myocarditis Foundations international Medical Advisory Board, made up of leading myocarditis researchers from around the world, voted to award a fellowship grant to Dr. Bode after selecting his application from a distinguished field of candidates.

Dr. Bodes research project is titled Role of PAR-1 in a Mouse Model of Viral Myocarditis Below is a laymans summary of his research:

“It is estimated that myocarditis causes up to 20% of sudden death in adults less than 40 years of age, and Coxsackievirus B3 is considered to be one of the most important causes of myocarditis. I am trying to better understand the mechanisms that protect the heart from viral myocarditis. In particular, I am going to identify the role of the blood coagulation system in the regulation of the immune response against viral myocarditis. We have previously shown that a protein called PAR-1 that gets activated by the clotting system plays an important role in protecting mice from Coxsackievirus B3 infection. I recently found that especially PAR-1 in cardiomyocytes, which are the cells in the heart that are contracting, plays an important role in protecting the heart from the virus. I would now like to understand the pathways inside the cells that lead to protection, by doing cell culture experiments with cardiomyocytes. This will involve stimulating the cells with a PAR-1 activator to see if this causes them to produce proteins that can protect the cells from the virus. I will also add inhibitors of different pathways to examine which pathway is most important. In addition, I will use mice that are lacking PAR-1 in cardiomyocytes to observe the effects of the virus infection in the absence of PAR-1. I expect these mice to be sicker, to have a worse heart function, and to produce less proteins that protect them from the virus. By understanding the mechanism of viral myocarditis in detail, we may be able to improve the current therapy or establish novel therapies to protect the heart from viral infections..” -Summary by Dr. Bode

The Myocarditis Foundation is honored to work with Dr. Bode and the University of North Carolina, furthering the expansion of myocarditis research. It is the Foundations goal to build a greater understanding of the disease and find better ways to diagnose, treat, and ultimately prevent myocarditis from taking more lives.

The Myocarditis Foundation would like to thank all the families, businesses, and organizations that have supported the Foundation in 2014. It is with their generosity and support that these research grants are able to be awarded each year.

For more information regarding the Myocarditis Foundation and its grant program, please visit: www.myocarditisfoundation.org.


The Myocarditis Foundation Announces its 2013 Grant Recipient for the 2014/15 Grant Cycle

The Myocarditis Foundation is pleased to announce that it will be funding a research fellowship grant for the 2014/15 grant cycle. The Myocarditis Foundation will be funding a research grant awarded to Dr. Yuji Nagatomo of the Cleveland Clinic in the amount of $35,000. Dr. Nagatomo is under the mentorship of Dr. Wilson Tang of the Cleveland Clinic.

The Myocarditis Foundation, an international non-profit organization founded in 2005, is dedicated to increasing awareness and hastening progress in understanding this rare disease.Myocarditis is a disease that is marked by inflammation and scarring of the heart muscle, which can progress rapidly to heart failure and death or heart transplantation.

The Myocarditis Foundation announced in its third quarter 2013 that it was accepting grant applications until December 2013. Their international Medical Advisory Board, made up of leading myocarditis researchers from around the world, voted to award a fellowship grant to Dr. Nagatomo after selecting his application from a distinguished field of candidates.

Dr. Nagatomos research project is titled Autoimmunity in Suspected Myocarditis and Recent-Onset Cardiomyopathy: The significance of IgG3 autoantibody against 1 adrenergic receptors Below is a laymans summary of his research.

“Over the years, there has been extensive research work surrounding the presence of antibodies that attack the components of the adrenaline system, which may directly or indirectly affect the function of the heart. Termed autoantibodies, they may stimulate the system and activate the flight and fight response that drives the heart to get weaker over time. Preliminary findings have suggested that removal of one specific type of autoantibodies, IgG3, appears to be most effective in facilitating recovery of heart function. The objective of this study is to determine how common this subtype of autoantibody that acts against the adrenergic system is found in patients with new-onset heart failure or suspected myocarditis, and to see how these autoantibodies (and its subtype) directly influence the adrenaline system by looking at how they stimulate the blood cells. We believe that this research will provide novel insight into the pathology of myocarditis and lead to the development of new treatment modality for this potential therapeutic target.”

– Summary by Dr. Nagatomo

Dr. Yuji Nagatomo of the Cleveland Clinic

Dr. Yuji Nagatomo of the Cleveland Clinic

The Myocarditis Foundation is honored to work with Dr. Nagatomo and the Cleveland Clinic, furthering the expansion of myocarditis research. It is the Foundations goal to build a greater understanding of the disease and find better ways to diagnose, treat, and ultimately prevent myocarditis from taking more lives.

The Myocarditis Foundation has also approved to co-sponsor a research grant with the American Heart Association (AHA), but the 2013 end-of-year AHA grant applications did not match the guidelines put forth by the Myocarditis Foundation. New grant applications will be submitted in the spring of 2014, and hopefully one will meet the Myocarditis Foundations Medical Advisory Board research guidelines. It is the Myocarditis Foundations goal to award two grants for the 2014/15 grant cycle.

The Myocarditis Foundation would like to thank all the families, businesses, and organizations that have supported the Foundation in 2013. It is with their generosity and support that these research grants are able to be awarded each year.


The Myocarditis Foundation Awards Two Research Grants in 2012

The Myocarditis Foundation is pleased to announce that it will be funding two research fellowship grants for the 2013/14 grant cycle. The Myocarditis Foundation will be funding a research grant awarded to Dr. Chandirasegaran Massilamany of the University of Lincoln in the amount of $35,000 and have co-sponsored a grant with the American Heart Association awarded to Brian Avanzino of the University of California Davis in the amount of $50,000, half of which will be funded by the Myocarditis Foundation.

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Dr. Kevin Quinn of the University of California in Los Angeles

Awarded grant in 2012

Identifying Antiviral Agents to Treat Coxsackievirus Myocarditis

Dr. Kevin Quinn of the University of California in Los Angeles

In support of a long-term goal of identifying potent and tolerable antiviral drugs to prevent enteroviral myocarditis, our project has the following 3 goals:

  1. To identify the compounds which most actively inhibit coxsackievirus replication in tissue culture cells
  2. To identify the mechanism of action that allows these viral inhibitors to prevent coxsackievirus from completing its lytic cycle
  3. To test the most active inhibitors in a mouse model of coxsackievirus myocarditis. Those effective in inhibiting coxsackievirus infection in animal models could in turn be evaluated towards application in human patients.

Dr. Laure Case of the University of Vermont

Awarded grant in 2012

Chromosome Y Regulates usceptibility to Coxsackievirus
B3-induced Myocardtis

Dr. Laure Case of the University of Vermont

The experiments proposed in this fellowship will identify the critical cell types, for example cardiomyocytes and/or immune cells, which influence myocarditis susceptibility in the consomic mice. Thisdata will provide the necessary cellular link for future work that tests the hypothesis that ChrY dependent regulation of genes on other chromosomes is evolutionarily conserved, and that this mechanism influences myocarditis susceptibility among male mice. This is a very novel and exciting area of genetic research that will reveal ChrYs contribution to phenotypic differences that directly impact susceptibility to myocarditis and allow for the identification of genes and pathways that can be targeted for mechanistic studies and therapeutic intervention.


Dr. Alan Valaperti of the University of Health Network at the University of Toronto in Canada

Awarded grant in 2011

IL-1 Receptor-associated Kinase 4 (IRAK4) Epigentically Modulates Nod2- and MDA5- dependent Protection in Viral Myocarditis

Dr. Alan Valaperti of the University of Health Network at the University of Toronto in Canada

First we observed that the major cell population infiltrating into the inflamed heart of Coxsackie virus B3 (CVB3)-inoculated IRAK4 deficient mice were macrophages. We were able to show that upon in vitro infection with Coxackievirus B3 (CVB3), IRAK4 down-regulated IFN- and IFN-, but not IFN-, exclusively in macrophages, but not in myeloid dendritic cells or plasmacytoid dendritic cells. Simultaneous down-regulation of IFN- and IFN-, which means up-regulation of IFN- and IFN- in IRAK4 deficient cells, was enough to dramatically reduce viral replication in infected macrophages.

In addition, IRAK4 showed unique functions that were only partially shared with its upstream molecule MyD88. In particular, IRAK4 deficiency showed better stability of MDA5, which is an important cytoplasmic receptor to recognize Coxackievirus genome to mount an interferon-dependent anti-viral response. On the contrary, CVB3-infected wild-type macrophages showed a relevant degradation of MDA5 few hours after infection, whereas MyD88 deficient cells showed degradation of MDA5 in a later stage. This resulted in higher viral protection in IRAK4 deficient cells compared to wild-type or MyD88 deficient counterparts.


Dr. Kathleen Simpson of Washington University in St. Louis, MO

Awarded grant in 2010

Autoimmunity in Pediatric Myocarditis: A Pilot Study

Dr. Kathleen Simpson of Washington University in St. Louis, MO

The relationship of autoimmunity in the pathophysiology and outcomes of pediatric myocarditis is unknown. Through the collaboration of regional pediatric hospitals encompassing the states of Missouri, Oklahoma, and Nebraska, we plan to determine the relationship of autoimmunity to outcomes in previously and newly diagnosed pediatric myocarditis. In addition, we will use MRI of the heart to determine specific findings in children and the role of MRI in disease progression and prognosis for children with myocarditis. Improving the understanding of patient immune reaction in myocarditis may lead to improvement in prognosis and treatment in children.


Dr. Byung Kwan Lim of the University of California in San Diego

Awarded grant in 2009

The Role of Dystrphin in Enterovirus Induced Viral Myocarditis

Dr. Byung Kwan Lim of the University of California in San Diego

Specific Aim1. Determine whether cardiac myocyte-specific, inducible expression of enterovirus protease 2A in the dystrophin knock-in adult mouse heart can prevent myocyte sarcolemmal membrane disruption and the subsequent development of cardiomyopathy.

Hypothesis: Dystrophin knock-in can prevent mycoyte sarcolemmal membrane disruption through inhibition of dystrophin cleavage by enterovirus protease 2A.

Expected Results: We will generate DysKI/2A/MCM triple transgenic mice to determine the effect of cleavage-resistant dystrophin in cardiac-specific inducible expression of enterovirus protease 2A.

Specific Aim2. Determine whether knock-in of dystrophin that prevent protease 2A cleavage of dystrophin can protect against CVB3 infection mediated cardiac myocyte damage and myocarditis.

Hypothesis: Dystrophin knock-in reduces dystrophin cleavage and sarcolemmal membrane disruption after CVB3 infection.

Expected Results: We generated inbred Balb/C DysKI mice to determine whether DysKI mice have less sarcolemmal membrane disruption and myocyte damage in CVB3 infection. Preliminary data showed no significant difference between DysKI and littermate controls. There are similar virus titer and Evans blue dye uptake percent. However, Balb/C mice have high susceptibility to CVB3 and immune response. To prove a mechanical effect of virus infection we will generate less susceptible inbred C3H background DysKI mice.


Dr. David Marchant of the University of British Columbia in Vancouver, Canada

Awarded grant in 2009

Discovering and Understanding Virus-Host Factor Interactions for Treatment of Viral Myocarditis

Dr. David Marchant of the University of British Columbia in Vancouver, Canada

We showed that virus signaling during infection originated from, and converge upon, dominant signaling nodes.This work, which employed several signaling inhibitors to investigate signaling networks, identified those target whose inhibition most effectively inhibited viral replication; the nodes.

We concluded that by targeting the dominant signaling nodes that are required for viral replication we could, hypothetically, discover the most effective target for treatment of CVB3 infection. This is the first work of its kind and should provide new avenues for investigation of the most effective antivirals for treatment of virally induced myocarditis.


Dr. Silvio Antoniak of the University of North Carolina in Chapel Hill

Awarded grant in 2009

Thrombin-PAR-1 Signaling in Viral Myocarditis

Dr. Silvio Antoniak of the University of North Carolina in Chapel Hill

I conclude that PAR-1 activation is essential in the early phase of virus infection to manage an effective immune response against CVB3. This response is maintained by a successful recognition of virus antigens by the TLR-3 pathway and a PAR-1 dependent NK cell activation. The altered immune reaction in PAR-1-/- mice leads to uncontrolled virus replication and later to an over-bursting immune response, aberrant cardiac remodeling leading to cardiac dysfunction after CVB3 infection.


Dr. Susan Wollersheim of the University of California in Los Angeles

Awarded grant in 2008

Cellular and Viral Determinants of Neonatal Group B
Coxsackievirus Myocarditis

Dr. Susan Wollersheim of the University of California in Los Angeles

Sequence comparisons of more recently circulating CVB1 and CVB3 virus 5UTR and stemloop 2 folding patterns reveal that more recently circulating CVB1 and CVB3 viruses are more similar to each other than to their prototype viruses from the 1940s. The area of highest divergence from protoype of each CVB was within the stemloop 2 structure, which has previously been identified as a genomic determinant in CVB cardiovirulence [11]; this may indicate why the newer strain of CVB1 was more cardiovirulent than ever described previously. This new CVB1-Chi07 also has larger plaque size than CVB1-Conn5 which correlates with a higher viral replication and titer [12]. The CVB1-Chi07 shows a slower rate of growth and lower peak titer than all of the CVB3 viruses assessed. In vitro mouse models to compare these CVB1 viruses have been initiated with one experiment which indicates that CVB1-Chi07 is much more virulent than CVB1-Conn5, however further studies and data will be collected to verify this.

IRES transactivating protein identification is preliminary at this time, but the three proteins that have been identified are involved in cellular translation. Further studies of confirmation are underway and future experiments will be performed with mouse myocyte proteins.


Dr. Bettina Heidecker of the University of Miami

Awarded grant in 2007

Gene Expression Profiling for Detection of Myocarditis

Dr. Bettina Heidecker of the University of Miami

The overall goal of this study is to improve diagnostic sensitivity for detection of myocarditis by endomyocardial biopsy derived transcriptomic biomarkers and to evaluate peripheral blood mononuclear cells as possible surrogates of heart tissue.


Dr. Daniela Cihakova of Johns Hopkins University

Awarded grant in 2007

The Role of Monocytes in Autoimmune Myocarditis

Dr. Daniela Cihakova of Johns Hopkins University

We have assembled evidence that EAM is driven in part by the Th17 pathway in the mouse; however, in the absence of IL-17A an equally severe disease can be driven through the Th1 pathway. It is not yet known whether IL-17 plays a similarly dominant role in the pathogenesis of human myocarditis. Given a lack of immunomodulatory treatments for myocarditis, blocking of the IL-23/IL-17 pathway could be very attractive option. Thus, in myocarditis different pathways can result in comparable disease (Cihakova et al., 2008)?