| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5586856 | Cytokine | 2017 | 7 Pages |
Abstract
Numerous inflammatory cytokines and chemokines play a role in LCH. Of those, more specific ones reflect the disease extent (MS vs. SS and MS+ vs. MSâ) or the BRAF V600E mutation status. It is thought that the most responsible cytokines and chemokines involved in the poor outcome may become future candidate therapeutic targets in LCH.
Keywords
NGFCCLBRAF V600EHGFSCFGM-CSFM-CSFCC-chemokine ligandIL-1RACC-chemokine receptorPDGFCXC-chemokine ligandOPNCXCLLCHMGCsFGFMultisystemECDCCRLIFTNFnatural killersIL-2RIL-1 receptor antagonistOsteopontininterferonIFNinterleukinInterleukin-18Erdheim–Chester diseasestandard errorSerumMultinucleated giant cellsCytokineMIFstem cell growth factorHepatocyte growth factorleukemia inhibitory factorMacrophage migration inhibitory factorgranulocyte-macrophage colony-stimulating factorgranulocyte colony-stimulating factorVascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)nerve growth factorfibroblast growth factorStem Cell FactorG-CSFtumor necrosis factorTRAILTNF-related apoptosis-inducing ligandmacrophage colony-stimulating factorsoluble IL-2 receptorodds ratioLangerhans cell histiocytosisChemokine
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Authors
Akira Morimoto, Yukiko Oh, Sachie Nakamura, Yoko Shioda, Tomomi Hayase, Toshihiko Imamura, Kazuko Kudo, Shinsaku Imashuku, on behalf of the Japan Langerhans cell histiocytosis Study Group on behalf of the Japan Langerhans cell histiocytosis Study Group,