2019
Ruxolitinib, a selective JAK1/2 inhibitor, for the treatment of serious diseases caused by Staphylococcus aureus superantigens
Carnes H, Mehrkens B, Stegman M, Rajagopalan G. Ruxolitinib, a selective JAK1/2 inhibitor, for the treatment of serious diseases caused by Staphylococcus aureus superantigens. The Journal Of Immunology 2019, 202: 190.34-190.34. DOI: 10.4049/jimmunol.202.supp.190.34.Peer-Reviewed Original ResearchSystemic inflammatory response syndromeMulti-organ failureT cellsHLA-DR3 transgenic miceHLA class II moleculesVehicle-treated miceVivo studiesInflammatory response syndromeT cell subsetsToxic shock syndromeJAK 1/2 inhibitorSelective JAK1/2 inhibitorClass II moleculesStaphylococcus aureusDose-dependent mannerSerious diseaseJanus kinaseIL-17Response syndromeOrgan failureJAK1/2 inhibitorActivation markersCell subsetsShock syndromeIL-2
2016
HLA-DR3 transgenic mice expressing Nur77-GFP reveal early and robust activation of T cells by superantigens during Staphylococcus aureus pneumonia.
Rajagopalan G, Karau M, Krogman A, Patel R, David C. HLA-DR3 transgenic mice expressing Nur77-GFP reveal early and robust activation of T cells by superantigens during Staphylococcus aureus pneumonia. The Journal Of Immunology 2016, 196: 66.9-66.9. DOI: 10.4049/jimmunol.196.supp.66.9.Peer-Reviewed Original ResearchSAg staphylococcal enterotoxin BT cell activationStaphylococcus aureus pneumoniaT cellsCell activationAureus pneumoniaStaphylococcal pneumoniaSerum cytokine/chemokine levelsCytokine/chemokine levelsHLA-DR3 transgenic miceT-cell activation markersEarly T cell activation markerRole of superantigensCell activation markersT cell subsetsTiming of administrationS. aureus strainsStaphylococcal enterotoxin BChemokine levelsDifferent time pointsHLA-DR3Activation markersCell subsetsCD69 expressionExperimental pneumonia
2007
Delineating the Roles of CD4+ and CD8+ T Cell Subsets in the Pathogenesis of Spontaneous Autoimmune Diabetes Using HLA-DQ8 Transgenic Mice
Rajagopalan G, Mangalam A, Kudva Y, David C. Delineating the Roles of CD4+ and CD8+ T Cell Subsets in the Pathogenesis of Spontaneous Autoimmune Diabetes Using HLA-DQ8 Transgenic Mice. Clinical Immunology 2007, 123: s71. DOI: 10.1016/j.clim.2007.03.379.Peer-Reviewed Original ResearchDistinct local immunogenic stimuli dictate differential requirements for CD4+ and CD8+ T cell subsets in the pathogenesis of spontaneous autoimmune diabetes
Rajagopalan G, Mangalam A, Sen M, Kudva Y, David C. Distinct local immunogenic stimuli dictate differential requirements for CD4+ and CD8+ T cell subsets in the pathogenesis of spontaneous autoimmune diabetes. Autoimmunity 2007, 40: 489-496. PMID: 17966038, DOI: 10.1080/08916930701649836.Peer-Reviewed Original ResearchConceptsIncidence of diabetesPathogenesis of T1DRat insulin promoterTransgenic mouse modelMouse modelHLA-DQ8 transgenic miceMurine type 1 diabetesDouble transgenic mouse modelMHC class II associationsLocal inflammatory stimuliSpontaneous autoimmune diabetesT cell subsetsClass II associationsType 1 diabetesAutoimmune diabetesImmunogenic stimulusProinflammatory cytokinesCell subsetsCostimulatory moleculesTNF-alphaT cellsInflammatory stimuliDiabetesTransgenic miceCD4