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Roles of toll‐like receptor 4 signalings in maturation and survival of bone marrow‐derived dendritic cells
Author(s) -
Kim Jee Youn,
Kim Hwan Mook,
Kang Jong Soon,
Park Song Kyu,
Roh Eunmiri,
Kim Yeon Jin,
Song Sukgil,
Kim Youngsoo,
Han SangBae
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.382
Subject(s) - mapk/erk pathway , tlr4 , p38 mitogen activated protein kinases , toll like receptor , kinase , microbiology and biotechnology , bone marrow , dendritic cell , receptor , downregulation and upregulation , chemistry , cancer research , signal transduction , immunology , biology , medicine , innate immune system , immune system , gene , biochemistry
Lipoplysacchride (LPS) signals to downstream effectors such as nuclear factor‐kappaB (NF‐kB) and mitogen‐activated protein kinases (MAPK) by using toll‐like receptor 4 (TLR4). However, their specific roles in survival and maturation of NF‐kB (TPCK), ERK (PD98059), p38 (SB203658) and Jun kinase (SP600125) differentially affect DC survival and maturation. Immature DCs were generated from bone marrow precursors by using 2 ng/ml of GM‐CSF. On day 8 of culture, non‐adherent and loosely adherent cells, i.e., immature DCs, were harvested from cultures and further activated with LPS for 1 day. TPCK impaired DC maturation without affecting their survival. On the other hand, SB203658 and PD98059 decreased survival, but not maturation, of DCs. Neither maturation nor survival was affected by SP600125. These results implicate that TLR4 signaling induces DC maturation through ERK and p38 activation, while NF‐kB activation is required to maintain DC survival.