RORγt-specific transcriptional interactomic inhibition suppresses autoimmunity associated with T H 17 cells
Copyright policy )RORγt-specific transcriptional interactomic inhibition suppresses autoimmunity associated with T H 17 cells
Significance T H 17 cells are a subset of CD4 + T helper cells that secrete the cytokine IL-17 and play a role in autoimmunity. RORγt is identified as a key transcription factor driving the T H 17 differentiation. Sequence analysis indicated that transcription factor contains several conserved DNA-binding domain and isotype-specific domain that we termed transcription modulation domain (TMD). We designed a novel therapeutics, tRORγt-TMD, to deliver RORγt-TMD efficiently into the nucleus of the cells that regulates T H 17 cell functions and T H 17-mediated autoimmune diseases. With the same concept, tTbet-TMD also can regulate T H 1 functions. In conclusion, tRORγt-TMD/tTbet-TMD can be novel and highly specific therapeutics for the treatment of T H 17/T H 1-mediated inflammatory disease and further allows us to discover new function of RORγt/Tbet in animals without genetic alteration.
- Yale University United States
- Yonsei University Medical Library Korea (Republic of)
- Yonsei University Korea (Republic of)
- Seoul National University Korea (Republic of)
- Yonsei University Health System Korea (Republic of)
Encephalomyelitis, Autoimmune, Experimental, Nuclear Receptor Subfamily 1, Cell Differentiation/genetics, Cell Nucleus/immunology*, Th17 Cells/immunology*, 610, Spinal Cord/pathology, Cell Nucleus/pathology, Rheumatoid/immunology*, Th1 Cells/pathology, Arthritis, Rheumatoid, Mice, Cell Differentiation/immunology*, Group F, 616, Animals, Humans, Experimental/pathology, Th1 Cells/immunology, Rheumatoid/therapy, Member 3/immunology*, TH17, Experimental/genetics, Encephalomyelitis, transcription factor, Cell Nucleus, Arthritis, TMD, autoimmunity, Rheumatoid/genetics, Experimental/immunology*, Cell Differentiation, Th17 Cells/pathology, Nuclear Receptor Subfamily 1, Group F, Member 3, Th1 Cells, Member 3/antagonists & inhibitors, HEK293 Cells, Spinal Cord, Member 3/genetics, Experimental/therapy, Spinal Cord/immunology, Th17 Cells, Rheumatoid/pathology, RORγt, Autoimmune, HeLa Cells
Encephalomyelitis, Autoimmune, Experimental, Nuclear Receptor Subfamily 1, Cell Differentiation/genetics, Cell Nucleus/immunology*, Th17 Cells/immunology*, 610, Spinal Cord/pathology, Cell Nucleus/pathology, Rheumatoid/immunology*, Th1 Cells/pathology, Arthritis, Rheumatoid, Mice, Cell Differentiation/immunology*, Group F, 616, Animals, Humans, Experimental/pathology, Th1 Cells/immunology, Rheumatoid/therapy, Member 3/immunology*, TH17, Experimental/genetics, Encephalomyelitis, transcription factor, Cell Nucleus, Arthritis, TMD, autoimmunity, Rheumatoid/genetics, Experimental/immunology*, Cell Differentiation, Th17 Cells/pathology, Nuclear Receptor Subfamily 1, Group F, Member 3, Th1 Cells, Member 3/antagonists & inhibitors, HEK293 Cells, Spinal Cord, Member 3/genetics, Experimental/therapy, Spinal Cord/immunology, Th17 Cells, Rheumatoid/pathology, RORγt, Autoimmune, HeLa Cells
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