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J Clin Pathol. 2013 Dec;66(12):1058-64. doi: 10.1136/jclinpath-2012-201286. Epub 2013 Aug 28.

M2-polarised macrophages in infantile haemangiomas: correlation with promoted angiogenesis.

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  • 1The 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.

Abstract

AIMS:

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.

AIMS:

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.

KEYWORDS:

Immunohistochemistry; Immunopathology; Molecular Pathology

PMID:
23986554
DOI:
10.1136/jclinpath-2012-201286
[PubMed - indexed for MEDLINE]
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