Targeted therapy guided by single-cell transcriptomic analysis in drug-induced hypersensitivity syndrome: a case report.
Doyoung KimTetsuro KobayashiBenjamin VoisinJay-Hyun JoKeiko SakamotoSeon-Pil JinMichael KellyHelena B PasiekaJessica L NaffJon H MeyerleIjeoma D IkpeamaGary A FahleFred P DavisSergio D RosenzweigJulie C AlejoStefania PittalugaHeidi H KongAlexandra F FreemanKeisuke NagaoPublished in: Nature medicine (2020)
Drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms (DiHS/DRESS) is a potentially fatal multiorgan inflammatory disease associated with herpesvirus reactivation and subsequent onset of autoimmune diseases1-4. Pathophysiology remains elusive and therapeutic options are limited. Cases refractory to corticosteroid therapy pose a clinical challenge1,5 and approximately 30% of patients with DiHS/DRESS develop complications, including infections and inflammatory and autoimmune diseases1,2,5. Progress in single-cell RNA sequencing (scRNA-seq) provides an opportunity to dissect human disease pathophysiology at unprecedented resolutions6, particularly in diseases lacking animal models, such as DiHS/DRESS. We performed scRNA-seq on skin and blood from a patient with refractory DiHS/DRESS, identifying the JAK-STAT signaling pathway as a potential target. We further showed that central memory CD4+ T cells were enriched with DNA from human herpesvirus 6b. Intervention via tofacitinib enabled disease control and tapering of other immunosuppressive agents. Tofacitinib, as well as antiviral agents, suppressed culprit-induced T cell proliferation in vitro, further supporting the roles of the JAK-STAT pathway and herpesviruses in mediating the adverse drug reaction. Thus, scRNA-seq analyses guided successful therapeutic intervention in the patient with refractory DiHS/DRESS. scRNA-seq may improve our understanding of complicated human disease pathophysiology and provide an alternative approach in personalized medicine.
Keyphrases
- drug induced
- single cell
- liver injury
- adverse drug
- rna seq
- endothelial cells
- case report
- genome wide
- randomized controlled trial
- cell proliferation
- signaling pathway
- rheumatoid arthritis
- induced pluripotent stem cells
- high throughput
- gene expression
- epithelial mesenchymal transition
- oxidative stress
- dna methylation
- risk assessment
- physical activity
- single molecule
- pi k akt
- wound healing
- cell cycle
- replacement therapy