Here, the authors show that combining γ9δ2 TCR-mediated metabolic and co-stimulatory stress targeting by chimeric NKG2D or anti-CD277 co-receptors shapes transcriptomic heterogeneity of engineered T cells and is associated with improved control of solid tumors.

Sharpe and colleagues devise a conditional gene deletion model in mice for rapid sequential, combinatorial and lineage-specific interrogation of gene function in hematopoietic cells.

Induced pluripotent stem cell (iPSC)-derived macrophages (iMACs) are being used to make chimeric antigen receptor (CAR) macrophages for immunotherapy. Here the authors design a second-generation macrophage-specific CAR by integrating CD3ζ and toll/IL-1R (TIR) domains resulting in an M1-polarized CAR-iMAC with increased antitumor functions.

Wu and colleagues identify gene networks and transcription factors that control the differentiation of stem-like CD8+ CAR T cells into effector or exhausted CD8⁺ CAR T cells.

Here, the authors show that combining γ9δ2 TCR-mediated metabolic and co-stimulatory stress targeting by chimeric NKG2D or anti-CD277 co-receptors shapes transcriptomic heterogeneity of engineered T cells and is associated with improved control of solid tumors.

Sharpe and colleagues devise a conditional gene deletion model in mice for rapid sequential, combinatorial and lineage-specific interrogation of gene function in hematopoietic cells.

Induced pluripotent stem cell (iPSC)-derived macrophages (iMACs) are being used to make chimeric antigen receptor (CAR) macrophages for immunotherapy. Here the authors design a second-generation macrophage-specific CAR by integrating CD3ζ and toll/IL-1R (TIR) domains resulting in an M1-polarized CAR-iMAC with increased antitumor functions.

Wu and colleagues identify gene networks and transcription factors that control the differentiation of stem-like CD8+ CAR T cells into effector or exhausted CD8⁺ CAR T cells.

Mandal and colleagues report how the chromatin modulator BRWD1 mediates extensive changes in 3D chromatin topology during B cell development by converting static to dynamic cohesin.

Iwawura et al. identify a noncanonical role for NOD1, independent from its CARD-mediated proteoglycan sensing. Interactions between NOD1 and STAT5 are required for optimal lymphopoiesis in response to homeostatic cytokines.

Cancer immunology research is diverse, uses cutting-edge technologies and continues to excite with its constantly evolving contribution to new therapeutic options, and not just for patients with cancer.