Pathogenic function of bystander-activated memory-like CD4+ T cells in autoimmune encephalomyelitis.
Ontology highlight
ABSTRACT: T cells generate antigen-specific immune responses to their cognate antigen as a hallmark of adaptive immunity. Despite the importance of antigen-specific T cells, here we show that antigen non-related, bystander memory-like CD4+ T cells also significantly contribute to autoimmune pathogenesis. Transcriptome analysis demonstrates that interleukin (IL)-1β- and IL-23-prime T cells that express pathogenic TΗ17 signature genes such as RORγt, CCR6, and granulocyte macrophage colony-stimulating factor (GM-CSF). Importantly, when co-transferred with myelin-specific 2D2 TCR-transgenic naive T cells, unrelated OT-II TCR-transgenic memory-like TH17 cells infiltrate the spinal cord and produce IL-17A, interferon (IFN)-γ, and GM-CSF, increasing the susceptibility of th
SUBMITTER: Lee HG
PROVIDER: S-EPMC6372661 | biostudies-literature | 2019 Feb
REPOSITORIES: biostudies-literature
ACCESS DATA