title: Increased B Regulatory Phenotype in Non-Metastatic Lymph Nodes of Node-Positive Breast Cancer Patients.
abstract: Tumour-draining lymph nodes (TDLNs) are centre in orchestrating the immune responses against cancer. The cellularity and lymphocyte subpopulations change in the process of cancer progression and lymph node involvement. B lymphocyte subsets and their function in breast cancer-draining lymph nodes have not been well elucidated. Here, we studied the influence of tumour metastasis on the frequencies of different B cell subsets including naïve and memory B cells as well as those which are known to be enriched in the regulatory pool in TDLNs of 30 patients with breast cancer. Lymphocytes were obtained from a fresh piece of each lymph node and stained for CD19 and other B cell-associated markers and subjected to flow cytometry. Our investigation revealed that metastatic TDLN showed a significant decrease in active, memory and class-switched B cells while the frequencies of B cells with regulatory phenotypes were not changed. However, CD27(hi) CD25(+) and CD1d(hi) CD5(+) B regulatory subsets significantly increased in non-metastatic lymph nodes (nMLNs) of node-positive patients compared with node-negative patients. Our data provided evidence that in breast cancer, metastasis of tumour to axillary lymph nodes altered B cell populations in favour of resting, inactive and unswitched phenotypes. We assume that the lymphatic involvement may cause an increase in a subset of regulatory B cells in non-metastatic lymph nodes.
authors.affiliation: Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.|Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: F
authors.initials: F
authors.lastname: Mehdipour
authors.affiliation: Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: M
authors.initials: M
authors.lastname: Razmkhah
authors.affiliation: Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: A
authors.initials: A
authors.lastname: Hosseini
authors.affiliation: Department of Pathology, Shiraz Central Hospital, Shiraz, Iran.
authors.forename: M
authors.initials: M
authors.lastname: Bagheri
authors.affiliation: Department of Pathology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: A
authors.initials: A
authors.lastname: Safaei
authors.affiliation: Department of Surgery, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: A-R
authors.initials: AR
authors.lastname: Talei
authors.affiliation: Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.|Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: A
authors.initials: A
authors.lastname: Ghaderi
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D016175:B-Lymphocyte Subsets / Q000276:immunology*; D060151:B-Lymphocytes, Regulatory / Q000276:immunology*; D001943:Breast Neoplasms / Q000276:immunology*; D044584:Carcinoma, Ductal / Q000276:immunology*; D002454:Cell Differentiation; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D007108:Immune Tolerance; D017578:Immunoglobulin Class Switching; D007156:Immunologic Memory; D016130:Immunophenotyping; D008198:Lymph Nodes / Q000276:immunology*; D008875:Middle Aged; D009362:Neoplasm Metastasis; D010641:Phenotype; D019139:Tumor Escape
chemical_list: D015703:Antigens, CD