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Identification of novel mimicry epitopes for cardiac myosin heavy chain-α that induce autoimmune myocarditis in A/J mice.
Myocarditis is one cause of sudden cardiac death in young adolescents, and individuals affected with myocarditis can develop dilated cardiomyopathy, a frequent reason for heart transplantation.
An epitope from Acanthamoeba castellanii that cross-react with proteolipid protein 139-151-reactive T cells induces autoimmune encephalomyelitis in SJL mice
It is demonstrated that both ACA 83-95 and PLP 139-151 generate antigen-specific cross-reactive CD4 T cells and the T cells secrete identical patterns of cytokines and induce EAE with a similar severity.
Intricacies of cardiac damage in coxsackievirus B3 infection: implications for therapy.
Evidence is provided to suggest that CVB3 infection accompanies the generation of cardiac myosin-specific CD4 T cells that can transfer the disease to naïve recipients, suggesting a role for CVB-mediated autoimmunity in the disease pathogenesis.
Autoimmunity in viral myocarditis
Antigenic mimicry between microbes and cardiac proteins causes autoimmunity in myocarditis, and characteristics of innate immunity associated with cardiac infection determine relevant epitope expression (cryptic epitopes).
miR-27b*, an oxidative stress-responsive microRNA modulates nuclear factor-kB pathway in RAW 264.7 cells
The data suggest that macrophage functions can be regulated by oxidative stress-responsive miRNAs by modulating the NF-kB pathway.
Coxsackievirus B3 infection leads to the generation of cardiac myosin heavy chain-α-reactive CD4 T cells in A/J mice.
The data suggest that CVB3, a bona fide pathogen of cardiovascular system that primarily infects the heart can lead to the secondary generation of autoreactive T cells and contribute to cardiac pathology.
Detection of cardiac myosin heavy chain-α-specific CD4 cells by using MHC class II/IA(k) tetramers in A/J mice.
Tetramers were created using approaches that involve covalent tethering of individual peptide sequences or exogenous loading of peptides into empty IA(k) molecules by peptide-exchange reaction and demonstrated that by flow cytometry (FC), Myhc-α 334-352 tetramers specifically bind myosin-reactive T cells.
Localization of CD8 T cell epitope within cardiac myosin heavy chain-α334-352 that induces autoimmune myocarditis in A/J mice.
New insights are provided as to how different immune cells can recognize the same antigen and inflict damage through different mechanisms as determined by histology and magnetic resonance microscope imaging.
Retinoic acid‐induced autoantigen‐specific type 1 regulatory T cells suppress autoimmunity
It is demonstrated that the induction of autoantigen‐specific Tr1 cells can prevent the development of autoimmunity.
Potential of urinary metabolites for diagnosing multiple sclerosis.
NMR analysis of urine permitted the identification of metabolites that differentiate experimental autoimmune encephalomyelitis-mice from healthy and MS drug-treated EAE mice, and demonstrate that urinary metabolites have significant promise for monitoring disease-progression, and response to treatment in MS patients.