title: M2-polarised macrophages in infantile haemangiomas: correlation with promoted angiogenesis.
abstract: OBJECTIVE
  The pathogenesis of infantile haemangiomas (IHs) is still far from clear despite the fact that they are common vascular tumours distinctive for their perinatal presentation, rapid growth during the first year of life and subsequent slow involution.
  
  
  OBJECTIVE
  To determine the role of M2-polarised macrophages in IHs.
  
  
  METHODS
  M2-polarised macrophages were initially identified in 20 specimens of IHs by both immunochemistry and immunofluorescence for CD68 and CD163. The immunopositive M2-polarised macrophages in different phases of IHs were quantified, and further analysed for their correlations with the expression levels of Ki67, vascular endothelial growth factor (VEGF) and macrophage colony-stimulating factor (M-CSF).
  
  
  RESULTS
  The infiltrating macrophages in proliferative IHs were predominantly CD68/CD163, thus of the M2-polarised phenotype, whereas the density of these cells was significantly decreased in the involuting IHs. The high density of M2-polarised macrophages in proliferative IHs was closely correlated with overexpression of M-CSF, one of the cytokines considered to induce macrophages to polarise towards an M2 phenotype. The infiltrating M2-polarised macrophages probably contributed to the proliferation and angiogenesis of haemangioma endothelial cells, as evidenced by their close correlations with the immunoreactivities of Ki67 and VEGF.
  
  
  CONCLUSIONS
  Results indicate that the infiltrating M2-polarised macrophages may contribute to the progression of IHs by promoting the angiogenic process.
authors.affiliation: The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, , Wuhan, China.
authors.forename: Feng-Qin
authors.initials: FQ
authors.lastname: Wang
authors.forename: Gang
authors.initials: G
authors.lastname: Chen
authors.forename: Jun-Yi
authors.initials: JY
authors.lastname: Zhu
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Jian-Gang
authors.initials: JG
authors.lastname: Ren
authors.forename: Hui
authors.initials: H
authors.lastname: Liu
authors.forename: Zhi-Jun
authors.initials: ZJ
authors.lastname: Sun
authors.forename: Jun
authors.initials: J
authors.lastname: Jia
authors.forename: Yi-Fang
authors.initials: YF
authors.lastname: Zhao
mesh_terms: D015703:Antigens, CD / Q000276:immunology / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology / Q000378:metabolism; D016764:Cell Polarity; D049109:Cell Proliferation; D018450:Disease Progression; D005260:Female; D005455:Fluorescent Antibody Technique; D006391:Hemangioma / Q000098:blood supply / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D019394:Ki-67 Antigen / Q000276:immunology* / Q000378:metabolism; D016173:Macrophage Colony-Stimulating Factor / Q000276:immunology* / Q000378:metabolism; D008264:Macrophages / Q000166:cytology / Q000276:immunology* / Q000502:physiology; D008297:Male; D009389:Neovascularization, Pathologic; D010641:Phenotype; D011379:Prognosis; D011956:Receptors, Cell Surface / Q000276:immunology / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000276:immunology* / Q000378:metabolism; D000098902:CD163 Antigen; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D019394:Ki-67 Antigen; D016173:Macrophage Colony-Stimulating Factor; D011956:Receptors, Cell Surface; D042461:Vascular Endothelial Growth Factor A; D000098902:CD163 Antigen; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C467484:VEGFA protein, human
keywords: Immunohistochemistry; Immunopathology; Molecular Pathology