Platelet-Activation Factor Receptor Induces Interleukin 10 Production through STAT3 Activation in Dendritic Cells
Platelet-Activation Factor Receptor Induces Interleukin 10 Production through STAT3 Activation in Dendritic Cells
Journal of Immunobiology (Hilaris Publishing S.L) has announced almost 50% discount on article processing charge to commemorate its 10th Anniversary.
Journal of Immunobiology is an open access, peer-reviewed journal that focuses and welcomes submissions on all aspects of Immunobiology, Immunology, Autoimmunity, Innate Immunity, Adaptive Immunity, immunization, Immunogenetics, Immune Disorders, Immunodeficiency, Immune inflammation, Immunoinformatics, Clinical Immunology, Allergy & Immunology, Clinical & Vaccine Immunology, Inflammatory Disorders, Autoimmune Disorders, Immunotherapy and Immunopathology of infectious, allergic and autoimmune disease etc.
It gives us great pleasure to announce the call for paper on the occasion of 10th Anniversary of the Journal at special and hefty discount of up to 50 % on one-time article processing charge. Prospective academicians and scientists are encouraged to utilize this opportunity to get their articles reviewed, processed and published at relatively faster pace and at lower charges. In addition to this, the authors who publish with us during the year-long celebrations will also be eligible for academic awards recommended by the editorial panel.
The Archive page contains wide variety of articles such as Research / Review / Case reports / short communication / Mini review / Prospective / Letter to Editors Etc. We would like introduce a Research article which has been spread to the widest audience of experts; and thus increased in readership, citations and altimetry score.
Abstract: The activation of the platelet-activating factor receptor (PAFR) is associated to a suppressor phenotype in macrophages and dendritic cells (DCs). In the present study, we investigated mechanisms underlying the production of the interleukin 10 (IL-10) through PAFR activation in murine DCs. For this purpose, BALB/c mice bone marrow derived DCs were differentiated by GM-CSF treatment and stimulated with LPS in the presence of the PAFR antagonist WEB2086. Signalling pathways downstream to TLR4 activation were investigated. We found that LPS stimulus induced PAFR ligands generation by DCs, but it did not affect the PAFR expression. The LPS-induced IL-10 production was found to be partially dependent of PAFR, since it was reduced in the presence of WEB2086. The IL-10 production through PAFR activation was independent on CREB and PPARγ, as the treatment with selective inhibitors of these pathways did not affect the IL-10 production. TLR4 adaptor molecules (MyD88 and TRIF) expression, MAPK, or NF-κB (p105/50 and p65 subunits) activation pathways were also excluded, since they were not affected by the treatment with WEB2086. The blockage of PAFR by WEB2086 down regulated the STAT3 (Tyr705) phosphorylation induced by LPS. Additionally, DCs treated with STAT3 inhibitor (S3I-201) showed reduced IL-10 production to the same levels observed in DCs treated with WEB2086. The requirement of STAT3 was confirmed in PAFR-KO DCs, since the STAT3 inhibition did not affect IL-10 production by these cells. Our data show an additional molecular mechanism whereby PAFR contributes to IL-10 production in DCs and support the importance of the PAFR activation in DCs phenotype and function.
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