Tolerogenic signals delivered by dendritic cells to T cells through a galectin-1-driven immunoregulatory circuit involving interleukin 27 and interleukin 10

Despite their central function in orchestrating immunity, dendritic cells (DCs) can respond to inhibitory signals by becoming tolerogenic. Here we show that galectin-1, an endogenous glycan-binding protein, can endow DCs with tolerogenic potential. After exposure to galectin-1, DCs acquired an inter...

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Detalles Bibliográficos
Autores principales: Ilarregui, J.M., Croci, D.O., Bianco, G.A., Toscano, M.A., Salatino, M., Vermeulen, M.E., Geffner, J.R., Rabinovich, G.A.
Formato: JOUR
Materias:
galectin 1
gamma interferon
granulocyte macrophage colony stimulating factor
interleukin 10
interleukin 27
ovalbumin
animal cell
antiinflammatory activity
article
CD4+ T lymphocyte
cell differentiation
cell stimulation
controlled study
cytokine production
cytokine release
dendritic cell
human
human cell
immunological tolerance
immunoregulation
inflammation
mouse
nonhuman
priority journal
protein expression
protein function
protein localization
signal transduction
T lymphocyte
upregulation
Animals
Antigens, CD40
Dendritic Cells
Encephalomyelitis, Autoimmune, Experimental
Female
Galectin 1
Gene Expression Regulation
Glycoproteins
Immune Tolerance
Interleukin-10
Interleukins
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Peptide Fragments
STAT3 Transcription Factor
T-Lymphocytes
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_15292908_v10_n9_p981_Ilarregui
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:Despite their central function in orchestrating immunity, dendritic cells (DCs) can respond to inhibitory signals by becoming tolerogenic. Here we show that galectin-1, an endogenous glycan-binding protein, can endow DCs with tolerogenic potential. After exposure to galectin-1, DCs acquired an interleukin 27 (IL-27)-dependent regulatory function, promoted IL-10-mediated T cell tolerance and suppressed autoimmune neuroinflammation. Consistent with its regulatory function, galectin-1 had its highest expression on DCs exposed to tolerogenic stimuli and was most abundant from the peak through the resolution of autoimmune pathology. DCs lacking galectin-1 had greater immunogenic potential and an impaired ability to halt inflammatory disease. Our findings identify a tolerogenic circuit linking galectin-1 signaling, IL-27-producing DCs and IL-10-secreting T cells, which has broad therapeutic implications in immunopathology.

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