A recent article by Dai et al. has shown that the transcription factor ZEB2 is required for B cells to become age-associated B cells (ABCs), a type of memory B cell that is linked to microbial immunity, autoimmunity, and metabolic disease.

In this work, we found that therapy-induced senescence (TIS) was associated with the activation of the terminal complement pathway evidenced by the increased tumor cell formation of C5b-9 and upregulation of complement regulatory proteins, especially CD59 and complement factor H. TIS was also associated with increased expression and secretion of C3.

Our work demonstrates that the CD10⁻ neutrophils in patients with non-Hodgkin's lymphoma are a relatively uniform, myeloid-derived suppressor cell–like cells subset with T-cell-suppressive capacities and immature features. Importantly, the frequency of CD10⁻ neutrophils is associated with disease development and progression.

Factors that regulate fibroblastic reticular cells (FRCs) in lymph nodes (LNs) are poorly understood. We identified that the transcription factor SpiB is a critical regulator of FRC functionality and subsequent immune responses in LNs.

In this study, we demonstrate that NK cells show reduced cytokine production and degranulation in the West Nile virus-infected central nervous system. This corresponded with an upregulation of inhibitory NK cell molecule, MHC-I, in the brain and downregulation in metabolic pathways associated with NK cell cytotoxicity. Overall, this study identifies a likely link between MHC-I inhibition of NK cells and metabolic reduction of their cytotoxicity during infection.