BackgroundImmunoglobulin-like transcript 4 (ILT4) is an inhibitory molecule involved in immune response and has recently been identified to be strongly inducible by IL-10. The aim of the present study was to examine the associations of ILT4 expression with clinicopathological characteristics and IL-10 expression in primary ductal and lobular breast cancer.MethodsWe studied the expression of ILT4 in 4 cancer cell lines, 117 primary tumor tissues and 97 metastatic lymph nodes from patients with primary ductal and lobular breast cancer by reverse transcription-polymerase chain reaction, western blot or immunohistochemistry analysis. Additionally, IL-10 expression was also investigated using immunohistochemistry in primary tumor tissues. Then the relationship between ILT4 expression and clinicopathological characteristics/IL-10 expression was evaluated.ResultsILT4 was highly expressed in all 4 human breast cancer cell lines on both mRNA and protein levels. In primary tumor tissues, ILT4 or IL-10 was expressed in the cell membrane, cytoplasm, or both; the positive rate of ILT4 and IL-10 expression was 60.7% (71/117) and 80.34% (94/117), respectively. ILT4 level was significantly correlated with IL-10 (r =0.577; p < 0.01). Furthermore, the expression of ILT4 or IL-10 was associated with less number of Tumor Infiltrating Lymphocytes (TILs) (p = 0.004 and 0.018, respectively) and more lymph node metastasis (p = 0.046 and 0.035, respectively).ConclusionOur data demonstrated the association of ILT4 and IL-10 expression in human breast cancer, suggesting their important roles in immune dysfunction and lymph node metastases.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1692652692107916

Podoplanin, a small mucin-type sialoglycoprotein, was recently shown to be involved in tumor progression. Podoplanin is overexpressed in cancer cells of various human malignancies, and recently, it is also detected in intratumoral stromal cells. We now appreciate that podoplanin plays a dual role in cancer: it can not only suppress tumor growth but also promote tumor progression. Researchers have identified several potential pathways invoked by podoplanin, which participate in the epithelial-to-mesenchymal transition, collective-cell migration, platelet activation and aggregation, and lymphangiogenesis, and thus regulate the tumor invasion and metastasis. Here, we discuss the current experimental and human clinical data on podoplanin to validate the multiple context-dependent functions in different microenvironments and to delineate the diverse regulatory mechanisms.

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