2023
A Nasal Inflammatory Cytokine Signature Is Associated with Early Graft-versus-Host Disease of the Lung after Allogeneic Hematopoietic Cell Transplantation: Proof of Concept
Ostrin E, Rider N, Alousi A, Irajizad E, Li L, Peng Q, Kim S, Bashoura L, Arain M, Noor L, Patel N, Mehta R, Popat U, Hosing C, Jenq R, Rondon G, Hanash S, Paczesny S, Shpall E, Champlin R, Dickey B, Sheshadri A. A Nasal Inflammatory Cytokine Signature Is Associated with Early Graft-versus-Host Disease of the Lung after Allogeneic Hematopoietic Cell Transplantation: Proof of Concept. ImmunoHorizons 2023, 7: 421-430. PMID: 37289498, PMCID: PMC10491477, DOI: 10.4049/immunohorizons.2300031.Peer-Reviewed Original ResearchConceptsBronchiolitis obliterans syndromeHematopoietic cell transplantationGraft-versus-host diseaseHematopoietic cell transplant recipientsTransient impairmentCell transplantationNasal inflammationNew-onset bronchiolitis obliterans syndromeChronic graft-versus-host diseaseMultiplex magnetic bead immunoassayNasal mucosal lining fluidAllogeneic hematopoietic cell transplantationMucosal lining fluidInflammatory cytokine signatureType 2 inflammationT cell activationMagnetic bead immunoassayNasal inflammatory responseRespiratory tract inflammationCounterregulatory moleculesBetween-group differencesIL-17ACytokine signatureBead immunoassayClinical criteria
2019
Recurrent pseudogout after therapy with immune checkpoint inhibitors: a case report with immunoprofiling of synovial fluid at each flare
Kim S, Bittar M, Kim H, Neelapu S, Zurita A, Nurieva R, Suarez-Almazor M. Recurrent pseudogout after therapy with immune checkpoint inhibitors: a case report with immunoprofiling of synovial fluid at each flare. Journal For ImmunoTherapy Of Cancer 2019, 7: 126. PMID: 31088575, PMCID: PMC6518723, DOI: 10.1186/s40425-019-0597-x.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitorsCheckpoint inhibitorsNivolumab infusionAdverse eventsIL-17 producing CD4Immune checkpoint inhibitor therapyImmune checkpoint inhibitor treatmentImmune-related adverse eventsPatients treated with nivolumabCD4+ T cellsAmount of IL-17Characterized immune cellsCheckpoint inhibitor treatmentPD-1 inhibitorsCheckpoint inhibitor therapyCrystal arthritisSynovial fluidRenal cell carcinomaAutoimmune inflammatory arthritisT helper 17Neutrophil-driven inflammationProphylactic colchicinePD-1Inhibitor therapyConclusionsThis case
2016
Protein stabilization improves STAT3 function in autosomal dominant hyper-IgE syndrome
Bocchini C, Nahmod K, Katsonis P, Kim S, Kasembeli M, Freeman A, Lichtarge O, Makedonas G, Tweardy D. Protein stabilization improves STAT3 function in autosomal dominant hyper-IgE syndrome. Blood 2016, 128: 3061-3072. PMID: 27799162, PMCID: PMC5201093, DOI: 10.1182/blood-2016-02-702373.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesDiterpenesDNA-Binding ProteinsHalf-LifeHeat Shock Transcription FactorsHerpesvirus 4, HumanHumansInterleukin-17Job SyndromeMiceModels, MolecularMutant ProteinsMutationPhosphotyrosineProtein BindingProtein StabilitySpleenSTAT3 Transcription FactorTranscription FactorsConceptsAutosomal dominant hyper-IgE syndromeSTAT3 mutationsPeripheral blood mononuclear cellsAD-HIESProtein stabilityEpstein-Barr virus-transformed BPY-STAT3Human peripheral blood mononuclear cellsHeat shock proteinsHyper-IgE syndromeSTAT3 target genesProtein half-lifeMouse splenocytesUpregulating heat shock proteinsAD-HIES patientsLevel of STAT3T cellsDominant-negative mutationsTreatment of human peripheral blood mononuclear cellsCD8<sup>+</sup> T cellsSTAT3 functionEpstein-Barr virus-transformed B cellsProtein functionHuman CD4<sup>+</sup>MRNA levels