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• W3189367864 abstract "HomeCirculationVol. 144, No. 5Response by Forte and Sattler to Letter Regarding Article, “Cross-Priming Dendritic Cells Exacerbate Immunopathology After Ischemic Tissue Damage in the Heart” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessLetterPDF/EPUBResponse by Forte and Sattler to Letter Regarding Article, “Cross-Priming Dendritic Cells Exacerbate Immunopathology After Ischemic Tissue Damage in the Heart” Elvira Forte, PhD Susanne SattlerPhD Elvira ForteElvira Forte https://orcid.org/0000-0002-5555-9122 The Jackson Laboratory, Bar Harbor, ME (E.F.). Search for more papers by this author and Susanne SattlerSusanne Sattler https://orcid.org/0000-0001-9932-4109 National Heart and Lung Institute, Imperial College London, UK (S.S.). Search for more papers by this author Originally published2 Aug 2021https://doi.org/10.1161/CIRCULATIONAHA.121.055584Circulation. 2021;144:e94–e95In Response:We thank Wang et al. for their interest and careful analysis of our basic research study showing that cross-priming dendritic cells have a pathologic role in persistent immunopathology after type 2 myocardial infarction.1 The authors touch on some critical aspects concerning the diverse and often apparently opposing roles of the immune system. Taken together, these mean that more studies are required to improve our understanding of the context-dependent and likely spatially and temporally controlled function of cross-priming dendritic cells before considering them a viable therapeutic target in human patients with myocardial infarction.We could not agree more with this assessment. In fact, we have observed—with a degree of frustration—that immunomodulatory treatments are being pushed through to clinical trials based on limited experimental evidence and without appropriately taking into account the intricacies of the immune response.2 This can lead to unsuccessful trial outcomes and the unfounded rejection of promising drug candidates.Wang et al. pointed out that (1) cross-priming is a fundamental immunologic process involved in maintaining baseline tissue homeostasis as well as boosting protective immune responses.3 It may thus also have beneficial effects, and blockade may be contraindicated, in particular for patients with concomitant immunodeficiencies or tumors as well as in heart disease with an infectious etiology; and (2) cross-priming dendritic cells are present throughout the body. The ability to specifically target cross-priming in the myocardium via cardiac-specific bioactive factors would avoid systemic effects and make such a therapy significantly more efficient and suitable for a larger range of patients.With our eyes on clinical translation, we agree with Wang et al. and thank them for providing a sensible clinical perspective. We have previously pointed out our recommendations for the design of future clinical studies using immunomodulation in heart disease,2 and these stand in this context and need to be investigated further. Our recommendations include putting particular emphasis on careful selection of the patient population to exclude those with prior immunologic and infectious disease. We also ask for careful consideration of (1) timing and duration of treatment with respect to the time-dependent role of the immune response after acute injury to block detrimental while maintaining beneficial effects, (2) immunologic effects of already present pharmacotherapy,4 and (3) potential complications of therapies targeting the immune system, including a suppression of protective immune responses against infections and tumors.With our basic research study, we provided the first report showing that dendritic cell cross-priming and the subsequent activation of cytotoxic T cells have a role in maintaining an inflammation–autoimmune loop in postischemic heart disease. We confirmed human relevance and translational potential by demonstrating an increase in cytotoxic T-cell numbers in human heart failure myocardium. We look forward to follow-up studies addressing subsequent questions, including some of those raised by Wang et al., to establish a solid basis for successful clinical translation.Disclosures None.Footnoteshttps://www.ahajournals.org/journal/circReferences1. Forte E, Perkins B, Sintou A, Kalkat HS, Papanikolaou A, Jenkins C, Alsubaie M, Chowdhury RA, Duffy TM, Skelly DA, et al.. Cross-priming dendritic cells exacerbate immunopathology after ischemic tissue damage in the heart.Circulation. 2021; 143:821–836. doi: 10.1161/CIRCULATIONAHA.120.044581LinkGoogle Scholar2. Panahi M, Papanikolaou A, Torabi A, Zhang JG, Khan H, Vazir A, Hasham MG, Cleland JGF, Rosenthal NA, Harding SE, et al.. Immunomodulatory interventions in myocardial infarction and heart failure: a systematic review of clinical trials and meta-analysis of IL-1 inhibition.Cardiovasc Res. 2018; 114:1445–1461. doi: 10.1093/cvr/cvy145CrossrefMedlineGoogle Scholar3. Embgenbroich M, Burgdorf S. Current concepts of antigen cross-presentation.Front Immunol. 2018; 9:1643. doi: 10.3389/fimmu.2018.01643CrossrefMedlineGoogle Scholar4. Panahi M, Vadgama N, Kuganesan M, Ng FS, Sattler S. Immunopharmacology of post-myocardial infarction and heart failure medications.J Clin Med. 2018; 7:E403. doi: 10.3390/jcm7110403CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails August 3, 2021Vol 144, Issue 5Article InformationMetrics Download: 97 © 2021 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.121.055584PMID: 34339310 Originally publishedAugust 2, 2021 PDF download" @default.
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