2023
HERV1-env Induces Unfolded Protein Response Activation in Autoimmune Liver Disease: A Potential Mechanism for Regulatory T Cell Dysfunction.
Subramanian K, Paul S, Libby A, Patterson J, Arterbery A, Knight J, Castaldi C, Wang G, Avitzur Y, Martinez M, Lobritto S, Deng Y, Geliang G, Kroemer A, Fishbein T, Mason A, Dominguez-Villar M, Mariappan M, Ekong U. HERV1-env Induces Unfolded Protein Response Activation in Autoimmune Liver Disease: A Potential Mechanism for Regulatory T Cell Dysfunction. The Journal Of Immunology 2023, 210: 732-744. PMID: 36722941, PMCID: PMC10691554, DOI: 10.4049/jimmunol.2100186.Peer-Reviewed Original ResearchConceptsAutoimmune hepatitisDe novo autoimmune hepatitisRegulatory T cell dysfunctionUnfolded protein responseNovo autoimmune hepatitisTregs of patientsAutoimmune liver diseaseIL-17A productionRegulatory T cellsT cell dysfunctionTreg suppressive functionExpression of RORCER stressEndoplasmic reticulum stressTreg plasticityLiver diseaseCell dysfunctionProtein response activationT cellsUnfolded protein response activationSuppressive functionIncreased expressionEffector propertiesReticulum stressPotential mechanisms
2018
Inflammasome Priming Mediated via Toll-Like Receptors 2 and 4, Induces Th1-Like Regulatory T Cells in De Novo Autoimmune Hepatitis
Arterbery AS, Yao J, Ling A, Avitzur Y, Martinez M, Lobritto S, Deng Y, Geliang G, Mehta S, Wang G, Knight J, Ekong UD. Inflammasome Priming Mediated via Toll-Like Receptors 2 and 4, Induces Th1-Like Regulatory T Cells in De Novo Autoimmune Hepatitis. Frontiers In Immunology 2018, 9: 1612. PMID: 30072988, PMCID: PMC6060440, DOI: 10.3389/fimmu.2018.01612.Peer-Reviewed Original ResearchToll-like receptor 2Monocytes/macrophagesAutoimmune hepatitisReceptor 2De novo autoimmune hepatitisRegulatory T cell phenotypeTumor necrosis factor αLate allograft dysfunctionLiver transplant subjectsNormal allograft functionNovo autoimmune hepatitisRegulatory T cellsLiver of patientsAdaptive immune mechanismsIFN-γ productionPro-inflammatory cytokinesT-cell phenotypeNecrosis factor αInflammatory signaling pathwaysAllograft dysfunctionAllograft functionDysfunctional TregsSpecific innateTransplant subjectsLiver transplantation