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Bone marrow B lymphocytes in multiple myeloma and MGUS: Focus on distribution of naïve cells and memory subsets.
Leukemia Research 2016 October
BACKGROUND/AIMS: Multiple myeloma (MM) is caused by proliferation of clonal plasma cells (cPCs) in bone marrow (BM), associated with numerical and functional defects in immune subsets. An impairment of B cell compartment is involved in onset/progression of the disease.
METHODS: By flow cytometry, we studied distribution of naïve/transitional (IgD(+)CD27(-)), memory unswitched (IgD(+)CD27(+)), memory switched (IgD(-)CD27(+)) and double negative (DN) (IgD(-)CD27(-)) B lymphocytes in BM of control subjects, and responding and relapsing patients.
RESULTS: We observed an increased percentage of IgD(+)CD27(+) B cells in healthy controls vs responding patients (p<0.05). Treated non complete responders exhibited an expanded DN compartment vs stringent complete responders (p=0.011); in turn IgD(+)CD27(-) subpopulation was larger in stringent complete responders vs other responding patients (p=0.006). None of the studied B cell subsets showed clonal restriction. Correlation analysis revealed negative correlations between naïve/transitional and DN B cells in all groups, except in newly diagnosed subjects.
CONCLUSIONS: This may be considered a feasible start point to explore the importance of B cells in the immunosuppressive MM BM microenvironment, correlating these findings with immunosenescence and therapy related increased risk of infection. Moreover, we propose a possible role of naïve/transitional and DN B cells as predictive markers in treated patients.
METHODS: By flow cytometry, we studied distribution of naïve/transitional (IgD(+)CD27(-)), memory unswitched (IgD(+)CD27(+)), memory switched (IgD(-)CD27(+)) and double negative (DN) (IgD(-)CD27(-)) B lymphocytes in BM of control subjects, and responding and relapsing patients.
RESULTS: We observed an increased percentage of IgD(+)CD27(+) B cells in healthy controls vs responding patients (p<0.05). Treated non complete responders exhibited an expanded DN compartment vs stringent complete responders (p=0.011); in turn IgD(+)CD27(-) subpopulation was larger in stringent complete responders vs other responding patients (p=0.006). None of the studied B cell subsets showed clonal restriction. Correlation analysis revealed negative correlations between naïve/transitional and DN B cells in all groups, except in newly diagnosed subjects.
CONCLUSIONS: This may be considered a feasible start point to explore the importance of B cells in the immunosuppressive MM BM microenvironment, correlating these findings with immunosenescence and therapy related increased risk of infection. Moreover, we propose a possible role of naïve/transitional and DN B cells as predictive markers in treated patients.
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