Figure 4.
Visualization of heterogeneity of CXCR2+ TAN infiltration in MM BM and FLs. Vectra Polaris staining was applied to formalin-fixed, paraffin-embedded sections from 12 patient samples (BM, n = 12; paired FL, n = 12). Representative Vectra images from 3 individual patient samples ([A-C, top rows] original magnification ×10; [A-C, bottom rows] original magnification ×30). Differential marker and cell distribution of CD138+ tumor cells and CD16+ cells. (A) The absence of CXCR2+ cells in BM with <1% malignant PCs (CD138+). (B) Accumulation of CXCR2+ neutrophils along with an increase of CD138+ cells in BM. (C) Extensive intratumoral infiltration of CXCR2+ neutrophils with increased CD138+ cells. (D-F) Representative visualizations of the 3 mature TAN populations: (1) CXCR2+CD10+TNFAIP3+ cells (D, arrow), (2) CXCR2+CD10+TNFAIP3– cells (E, arrow), and (3) CXCR2+CD10–TNFAIP3– cells (F, arrow). These data highlight the TAN heterogeneity and diversity within neutrophil populations in MM, emphasizing distinct phenotypic and functional subsets that may contribute variably to the TME.

Visualization of heterogeneity of CXCR2+ TAN infiltration in MM BM and FLs. Vectra Polaris staining was applied to formalin-fixed, paraffin-embedded sections from 12 patient samples (BM, n = 12; paired FL, n = 12). Representative Vectra images from 3 individual patient samples ([A-C, top rows] original magnification ×10; [A-C, bottom rows] original magnification ×30). Differential marker and cell distribution of CD138+ tumor cells and CD16+ cells. (A) The absence of CXCR2+ cells in BM with <1% malignant PCs (CD138+). (B) Accumulation of CXCR2+ neutrophils along with an increase of CD138+ cells in BM. (C) Extensive intratumoral infiltration of CXCR2+ neutrophils with increased CD138+ cells. (D-F) Representative visualizations of the 3 mature TAN populations: (1) CXCR2+CD10+TNFAIP3+ cells (D, arrow), (2) CXCR2+CD10+TNFAIP3 cells (E, arrow), and (3) CXCR2+CD10TNFAIP3 cells (F, arrow). These data highlight the TAN heterogeneity and diversity within neutrophil populations in MM, emphasizing distinct phenotypic and functional subsets that may contribute variably to the TME.

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