Tumor-induced T-cell actin synapse dysfunction mediated by inhibitory ligands is a common immunosuppressive mechanism used by hematologic and solid carcinoma cells. (A) IHC mean intensity expression ± SEM of CD200, CD274, CD276, and CD270 on intrafollicular CD20⁺ cells and CD279 expression on interfollicular CD3⁺ T cells in lymph tissue from FL patient samples compared with reactive lymph node samples (representative high-power 40× magnification and 63× inset images are shown). (B) Mean expression analysis ± SEM using an extremes of survival diagnostic FL TMA (>15-year long survival group compared with < 5-year short-survival patient group). (C) Representative high-power 40× magnification of CD270 expression on CD20⁺ tumor cells and CD279 expression on CD3⁺ T cells in TMA cores from pretransformation (FL) biopsy compared with each patient's transformation (DLBCL) biopsy. Comparison of expression between FL and transformation to DLBCL. (D) Autologous patient peripheral blood T-cell or healthy donor allogeneic T-cell F-actin synapse function with third-party healthy donor allogeneic B cells (+sAg) as APCs after primary coculture (24 hours) with primary tumor-infiltrated FL cells or DLBCLs (D), MM cell line RPMI8226 (E), SCC cell line VB6 (F), OC cell line SKOV3 (G) or a nonmalignant human ovarian epithelial cell line IOSE pretreated with neutralizing Abs (α). Colored columns show the mean T-cell synapse area ± SD from 6 donor functional screens. The confocal images show T-cell/APC conjugates after primary coculture with treated tumor cells (minimum n = 100 analyzed per experiment). Original magnification, 63×. *P < .05; **P < .01.