title: IL-13 as well as IL-4 induces monocytes/macrophages and a monoblastic cell line (UG3) to differentiate into multinucleated giant cells in the presence of M-CSF.
abstract: The formation of multinucleated giant cells (MGCs) from monocytes/macrophages is controlled by various cytokines whose crucial roles are not fully understood. In this study, we found that interleukin (IL)-13 as well as IL-4 induced peripheral blood monocytes (PBMs) and monoblastic cell line, UG3, to differentiate into MGCs in the presence of macrophage colony-stimulating factor (M-CSF), while IL-2, IL-7 or IL-10 did not. The presence of M-CSF was essential to this MGC formation, because IL-3 or granulocyte-macrophage colony-stimulating factor (GM-CSF) could not replace M-CSF. IL-4 and IL-13 have been known to inhibit the formation of osteoclast-like cells in the presence of stroma cells or osteoblastic cells. But in our system without stroma cells, IL-4 or IL-13 induced some of characteristics of osteoclasts such as tartrate-resistant acid phosphatase (TRAP) activity, vitronectin receptor (vit-R) expression and resorptive activity for hydroxyapatite, but not the expression of receptors for parathyroid hormone or calcitonin. These results suggest possible involvement of IL-4 and IL-13 in MGCs and osteoclasts development, and UG3 may be useful to further investigate the roles of IL-4 and IL-13 in the formation and physiology of MGCs, and the relationship between these MGCs and osteoclasts.
authors.affiliation: First Department of Internal Medicine, Kagawa Medical University, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ikeda
authors.forename: K
authors.initials: K
authors.lastname: Ikeda
authors.forename: K
authors.initials: K
authors.lastname: Sasaki
authors.forename: K
authors.initials: K
authors.lastname: Kawakami
authors.forename: K
authors.initials: K
authors.lastname: Hatake
authors.forename: Y
authors.initials: Y
authors.lastname: Kaji
authors.forename: H
authors.initials: H
authors.lastname: Norimatsu
authors.forename: M
authors.initials: M
authors.lastname: Harada
authors.forename: J
authors.initials: J
authors.lastname: Takahara
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D017886:Durapatite / Q000378:metabolism; D015726:Giant Cells / Q000166:cytology* / Q000201:enzymology / Q000378:metabolism; D006801:Humans; D018793:Interleukin-13 / Q000502:physiology*; D015847:Interleukin-4 / Q000502:physiology*; D007527:Isoenzymes / Q000378:metabolism; D016173:Macrophage Colony-Stimulating Factor / Q000502:physiology*; D008264:Macrophages / Q000166:cytology* / Q000187:drug effects; D009000:Monocytes / Q000166:cytology* / Q000187:drug effects; D018003:Receptors, Calcitonin / Q000096:biosynthesis; D018016:Receptors, Parathyroid Hormone / Q000096:biosynthesis; D019030:Receptors, Vitronectin / Q000096:biosynthesis; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D018793:Interleukin-13; D007527:Isoenzymes; D018003:Receptors, Calcitonin; D018016:Receptors, Parathyroid Hormone; D019030:Receptors, Vitronectin; D015847:Interleukin-4; D016173:Macrophage Colony-Stimulating Factor; D017886:Durapatite; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase