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Induction of interleukin‐10 expression through Fcα receptor in human monocytes and monocyte‐derived dendritic cells: role of p38 MAPKinase
Author(s) -
Pilette Charles,
Detry Bruno,
Guisset Amélie,
Gabriels Julie,
Sibille Yves
Publication year - 2010
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2009.120
Subject(s) - p38 mitogen activated protein kinases , monocyte , microbiology and biotechnology , chemistry , stimulation , immunology , mapk/erk pathway , biology , signal transduction , endocrinology
As previously reported by others for immunoglobulin (Ig)G, we observed that IgA can induce interleukin (IL)‐10 expression in human monocytes. In this study, we explored the molecular mechanisms of IL‐10 induction by IgA in monocytes and monocyte‐derived dendritic cells (MD‐DCs). Monomeric IgA induced IL‐10 production in monocytes and this production was further increased upon IgA cross‐linking. Similar IL‐10 responses were observed in monocytes and autologous MD‐DCs, and were inhibited (by ∼77%) by preincubation with a blocking mAb to FcαRI. IL‐10 induction by IgA correlated with activation of MAPKinases ERK1/2, p38 and JNK, whereas only p38‐inhibitor SB‐203580 inhibited IL‐10 induction. Upon IgA stimulation, AP‐1, NFκB and Sp1 transcription factors were activated and inhibitors of NFκB and of Sp1 suppressed IgA‐driven transcriptional activation of IL‐10. In addition, p38 MAPK activation appeared that it was required to control nuclear translocation of NFκB and Sp1 upon IgA stimulation. Therefore, in human monocytes and MD‐DCs the mechanisms of IL‐10 induction by IgA involve p38 MAPK‐dependent recruitment of both NFκB and Sp1.