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Role of CD30/CD30L Mediated Signaling in the Cross‐talk of Natural Killer Cells and Dendritic Cells
Author(s) -
Simhadri Vijaya Lakshmi,
Hansen Hinrich P,
Simhadri Venkateswara Rao,
Reiners Katrin,
Engert Andreas,
Von Strandmann Elke Pogge
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.22.1_supplement.1078.17
Subject(s) - microbiology and biotechnology , proinflammatory cytokine , dendritic cell , innate immune system , tumor necrosis factor alpha , interleukin 12 , biology , acquired immune system , inflammation , immunology , chemistry , immune system , cytotoxic t cell , in vitro , biochemistry
Natural killer (NK) cells are involved in innate immunity and also contribute to adaptive immunity, mediated through the cross‐talk with immature dendritic cells (iDCs). NK cells and iDCs play a major role at the site of inflammation. The activation of NK cells and maturation of iDCs is partially characterized on the molecular level, depends on the release of proinflammatory cytokines and receptor‐ligand interactions. Activated NK cells express CD30, and its ligand CD30L (CD153) is expressed on iDCs. We describe that engagement of CD30L contributes to the activation and maturation of dendritic cells. Stimulation of monocyte derived iDCs with immobilized CD30‐Fc results in the release of pro‐inflammatory cytokines TNFalpha, IL‐6 and IL‐8, and can be blocked by CD30 antibodies. Engagement of CD30L on iDCs leads to Reactive Oxygen Species (ROS) signaling; and the release of TNFalpha is blocked by MAP kinase inhibitors. Intriguingly, the interaction induced the expression of CD83, a specific marker for mature dendritic cells. We postulate that CD30‐CD30L interaction contributes to DC‐maturation, based on the induction of cytokine release. The better understanding of the molecules involved in the NK‐DC cross‐talk will provide a basis for the development of immunotherapeutics modulating the activity of NK cells and DCs. Research was supported by Deutsche Forschungsgemeinschaft (DFG) (STR 530/5‐1).