Tingible body macrophages (TBMs) were discovered more than 100 yr ago, yet their origins and cellular dynamics were unknown. Gurwicz et al. demonstrate that TBMs arise from lymph node–resident precursors and consume germinal center B cells by highly dynamic dendrites to prevent intracellular-content dissemination.

Sun et al. found that STAT3, activated by IL-10 and IL-21, regulates the terminal differentiation of effector CD8⁺ T cells in cancer and also plays an important role in effector CD8⁺ T cells in acute infection.

Petkova et al. identify a new Ptx3-positive immune-interacting subtype of lymphatic endothelial cells, iLECs, that drive oncogenic PI3K-driven lymphatic malformations. These cells produce chemokines that recruit pro-lymphangiogenic macrophages, which in turn promote pathological lymphatic vessel growth.

The authors use single-cell RNA-sequencing and TCR tracking to analyze blood and tumors from breast and ovarian cancer patients treated with PD-1 blockade and CDK4/6 inhibition. They find that both therapies are immunologically active and enhance T cell effector function and memory, respectively.

The WNK1 kinase is essential in B cells for T-dependent antibody responses because it is activated by signaling from BCR, CXCR5, and CD40, and regulates B cell migration, adhesion, T-dependent activation, and differentiation into germinal center B cells and plasma cells.

Yuling Li et al. identify selective expression of BCL6 in CCR6⁺ ILC3 among ILC family. BCL6 expression, promoted by intestinal microbiota, restrains the effector function and plasticity of CCR6⁺ ILC3.

We show suppression of CD4 effector T cell activation by Tregs is enforced through active mRNA translational control of the protein synthesis machinery. We show proof-of-concept therapeutic targeting of protein synthesis that leads to the mitigation of inflammatory responses invoked by Treg loss of function.