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J Leukoc Biol ; 110(6): 1023-1031, 2021 12.
Article in English | MEDLINE | ID: mdl-34643294

ABSTRACT

The 78-kDa glucose-regulated protein (GRP78) has extracellular, anti-inflammatory properties that can aid resolving inflammation. It has been established previously that GRP78 induced myeloid CD11c+ cell differentiation into distinct tolerogenic cells. This tolerance induction makes GRP78 a potential therapeutic agent for transplanted allogeneic grafts and autoimmune diseases, such as type 1 diabetes. In this research, it is revealed that rmGRP78-treated NOD mice bone marrow-derived CD11c+ cells (GRP78-DCs) highly expressed B7-H4 but down-regulated CD86 and CD40, and retained a tolerogenic signature even after stimulation by LPS. In the assessment of in vivo therapeutic efficacy after the adoptive transfer of GRP78-DCs into NOD mice, fluorescent imaging analyses revealed that the transfer specifically homed in inflamed pancreases, promoting ß-cell survival and alleviating insulitis in NOD mice. The adoptive transfer of GRP78-DCs also helped reduce Th1, Th17, and CTL, suppressing inflammatory cytokine production in vivo. The findings suggest that adoptive GRP78-DC transfer is critical to resolving inflammation in NOD mice and may have relevance in a clinical setting.


Subject(s)
Dendritic Cells/transplantation , Diabetes Mellitus, Type 1/immunology , Endoplasmic Reticulum Chaperone BiP , Immune Tolerance/immunology , Islets of Langerhans , Adoptive Transfer , Animals , Cell Differentiation/drug effects , Cell Differentiation/immunology , Dendritic Cells/immunology , Endoplasmic Reticulum Chaperone BiP/immunology , Endoplasmic Reticulum Chaperone BiP/metabolism , Endoplasmic Reticulum Chaperone BiP/pharmacology , Female , Islets of Langerhans/immunology , Islets of Langerhans/pathology , Mice , Mice, Inbred NOD , Pancreatitis/immunology
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