Inflammation in Target Organs

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: 29 August 2024 | Viewed by 1616

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Diabetes Unit, Department of Endocrinology and Metabolism, Hadassah Medical Center, The Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem 91120, Israel
Interests: insulin resistance; diabetes; lipid metabolism; glucose metabolism; disease prevention; obesity metabolic endocrinology; high fructose corn syrup; cardiovascular disease; obesity; telemedicine; telehealth; eHealth; mHealth; digital health; review; connected diabetes care; diabetes mellitus; glucose monitoring
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Special Issue Information

Dear Colleagues,

Various metabolic disorders affect target organs, such as the heart, kidneys, liver, blood vessels, and the brain. A substantial portion of the resultant damage can be attributed to inflammatory processes, compromising the functionality of these organs. Inflammation may induce organ fibrosis and precipitate irreversible damage. In this Special Issue, we will present an overview elucidating the inflammatory response, resultant damage, and future therapies to prevent and cure inflammation in target organs. We will explore the intricate relationship between inflammation and organ damage, drawing insights from studies on cell lines, animal models, and humans.

This Special Issue endeavors to underscore recent discoveries, elucidating the intricate mechanisms through which inflammation inflicts damage on the target organs. Its objective is to offer a comprehensive scope, encompassing research papers and reviews delineating specific interactions between target organs and inflammation. Such discernments possess the potential to profoundly shape future therapeutic strategies within this domain of study.

Prof. Dr. Itamar Raz
Roni Weinberg Sibony
Guest Editors

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  • inflammation
  • fibrosis
  • cardio-renal
  • vascular
  • liver
  • brain

Published Papers (1 paper)

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20 pages, 10992 KiB  
Investigation into Cardiac Myhc-α 334–352-Specific TCR Transgenic Mice Reveals a Role for Cytotoxic CD4 T Cells in the Development of Cardiac Autoimmunity
by Meghna Sur, Mahima T. Rasquinha, Kiruthiga Mone, Chandirasegaran Massilamany, Ninaad Lasrado, Channabasavaiah Gurumurthy, Raymond A. Sobel and Jay Reddy
Cells 2024, 13(3), 234; - 26 Jan 2024
Viewed by 1370
Myocarditis is one of the major causes of heart failure in children and young adults and can lead to dilated cardiomyopathy. Lymphocytic myocarditis could result from autoreactive CD4+ and CD8+ T cells, but defining antigen specificity in disease pathogenesis is challenging. [...] Read more.
Myocarditis is one of the major causes of heart failure in children and young adults and can lead to dilated cardiomyopathy. Lymphocytic myocarditis could result from autoreactive CD4+ and CD8+ T cells, but defining antigen specificity in disease pathogenesis is challenging. To address this issue, we generated T cell receptor (TCR) transgenic (Tg) C57BL/6J mice specific to cardiac myosin heavy chain (Myhc)-α 334–352 and found that Myhc-α-specific TCRs were expressed in both CD4+ and CD8+ T cells. To investigate if the phenotype is more pronounced in a myocarditis-susceptible genetic background, we backcrossed with A/J mice. At the fourth generation of backcrossing, we observed that Tg T cells from naïve mice responded to Myhc-α 334–352, as evaluated by proliferation assay and carboxyfluorescein succinimidyl ester staining. The T cell responses included significant production of mainly pro-inflammatory cytokines, namely interferon (IFN)-γ, interleukin-17, and granulocyte macrophage-colony stimulating factor. While the naïve Tg mice had isolated myocardial lesions, immunization with Myhc-α 334–352 led to mild myocarditis, suggesting that further backcrossing to increase the percentage of A/J genome close to 99.99% might show a more severe disease phenotype. Further investigations led us to note that CD4+ T cells displayed the phenotype of cytotoxic T cells (CTLs) akin to those of conventional CD8+ CTLs, as determined by the expression of CD107a, IFN-γ, granzyme B natural killer cell receptor (NKG)2A, NKG2D, cytotoxic and regulatory T cell molecules, and eomesodermin. Taken together, the transgenic system described in this report may be a helpful tool to distinguish the roles of cytotoxic cardiac antigen-specific CD4+ T cells vs. those of CD8+ T cells in the pathogenesis of myocarditis. Full article
(This article belongs to the Special Issue Inflammation in Target Organs)
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