Lymph Node CD169+ Macrophages in Anti-tumour Immunity
Dante Louie, Glory Leung, Yujia Lin and Shan Liao
Department of Microbiology, Immunology and Infectious Diseases, Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada
Background: Cancer metastasis is a leading cause of patient mortality and can relapse cancer post-treatment. Preliminary studies demonstrated systemic metastasis increase when lymph nodes (LNs) were absent, suggesting LNs limit systemic metastasis. Thus, we studied the LN’s response to tumour cells in preventing metastasis. Past research showed CD169+ macrophages lining the subcapsular sinus captured most of the tumour antigens entering the LN.
Hypothesis: CD169+ macrophages limit systemic metastasis by capturing tumour antigens and inducing immune responses.
Methods: Using fluorescently labeled cancer cells (EO771 breast cancer and B16F10 melanoma) we looked into immune responses that could be causing a reduction in distant metastasis. To establish CD169+ macrophages’ role, we depleted them using clodronate liposome (CLL).
Results: Immunofluorescent staining showed tumour cells along collagen fibres while antigens co-localize with CD169+ macrophages at the B-cell follicles of the LN in the light zone of the germinal center.
When comparing tumour growth in CLL locally treated to systemically treated mice, local injection showed accelerated tumour growth, whereas systemic showed slower tumour growth compared to controls.
CLL treated groups showed increased frequency of distant metastases in lungs and ELISA showed heightened IgG responses in CLL groups compared to their controls.
Conclusion: Our results suggest CD169+ macrophages sequester tumour antigens and prevent humoral responses to inhibit tumour metastasis.
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