MicroRNA-17-92 regulates IL-10 production by regulatory T cells and control of experimental autoimmune encephalomyelitis

Autor: Lukas T. Jeker, Jeffrey A. Bluestone, Jonathan H. Esensten, Malika M. Morar, Wendy Rosenthal, Dimitri de Kouchkovsky
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Male
T-Lymphocytes
Epitopes
T-Lymphocyte

Lymphocyte Activation
T-Lymphocytes
Regulatory

Mice
Epitopes
0302 clinical medicine
T-Lymphocyte Subsets
Immunology and Allergy
Homeostasis
Encephalomyelitis
Cells
Cultured

Mice
Knockout

0303 health sciences
Antigen Presentation
Cultured
Bcl-2-Like Protein 11
Effector
Experimental autoimmune encephalomyelitis
CD28
hemic and immune systems
Regulatory
3. Good health
Interleukin-10
Interleukin 10
medicine.anatomical_structure
RNA
Long Noncoding

Adult
Heterozygote
Encephalomyelitis
Autoimmune
Experimental

Regulatory T cell
Cells
Knockout
Antigen presentation
Immunology
chemical and pharmacologic phenomena
Biology
Article
03 medical and health sciences
Experimental
Young Adult
Costimulatory and Inhibitory T-Cell Receptors
CD28 Antigens
Proto-Oncogene Proteins
microRNA
medicine
Animals
Humans
Antigens
030304 developmental biology
Autoimmune disease
Histocompatibility Antigens Class II
PTEN Phosphohydrolase
Membrane Proteins
medicine.disease
Peptide Fragments
MicroRNAs
T-Lymphocyte
Myelin-Oligodendrocyte Glycoprotein
Apoptosis Regulatory Proteins
Gene Deletion
030215 immunology
Autoimmune
Zdroj: De Kouchkovsky, D; Esensten, JH; Rosenthal, WL; Morar, MM; Bluestone, JA; & Jeker, LT. (2013). MicroRNA-17-92 regulates IL-10 production by regulatory T cells and control of experimental autoimmune encephalomyelitis. Journal of Immunology, 191(4), 1594-1605. doi: 10.4049/jimmunol.1203567. UC San Francisco: Retrieved from: http://www.escholarship.org/uc/item/4076w7zf
Journal of immunology (Baltimore, Md. : 1950), vol 191, iss 4
JOURNAL OF IMMUNOLOGY
Popis: microRNAs (miRNA) are essential for regulatory T cell (Treg) function but little is known about the functional relevance of individual miRNA loci. We identified the miR-17–92 cluster as CD28 costimulation dependent, suggesting that it may be key for Treg development and function. Although overall immune homeostasis was maintained in mice with miR-17–92–deficient Tregs, expression of the miR-17–92 miRNA cluster was critical for Treg accumulation and function during an acute organ-specific autoimmune disease in vivo. Treg-specific loss of miR-17–92 expression resulted in exacerbated experimental autoimmune encephalitis and failure to establish clinical remission. Using peptide-MHC tetramers, we demonstrate that the miR-17–92 cluster was specifically required for the accumulation of activated Ag-specific Treg and for differentiation into IL-10–producing effector Treg.
Databáze: OpenAIRE