Issues

Rita Colwell is a Distinguished University Professor at the University of Maryland at College Park and at Johns Hopkins University Bloomberg School of Public Health, and president of the Rosalind Franklin Society. She has authored or co-authored 20 books and more than 800 scientific publications, and throughout her career has focused on improving health outcomes across the world and highlighting the impacts of infectious diseases in drinking/bathing water. We recently spoke to Rita about her career and her thoughts about the future for women in science.

Peng et al. identify inositol polyphosphate 4-phosphatase type II (Inpp4b) as regulator of ILC1 and NK cell tissue residency.

Kufera et al. demonstrate that proliferative growth of cells infected with genome-intact HIV-1 is not limitless; rather, these cells seem to be at least partially refractory to TCR stimulation.

Nutrients interplay with Signal 1 (antigens), Signal 2 (co-stimulation), and Signal 3 (cytokines) to orchestrate T cell activation, differentiation, and function. This review highlights the signaling and functional effects of nutrients as Signal 4 in T cell–mediated immunity.

In this study, it was found that the inositol phosphatase INPP4B is required to sustain ILC1s in peripheral tissues and NK cells in the tumor microenvironment through activation of AKT.

Lung resident memory CD8⁺ T cells (T_RM) control heterosubtypic influenza infection and potentially cancer. We show that thorax-targeted irradiation depletes lung T_RM and diminishes protection, but spares circulating memory CD8⁺ T cells that can be boosted to regenerate lung T_RM.

This study illuminates that TRPV2 augments B cell activation and function through membrane depolarization and cytoskeletal remodeling. Consequently, TRPV2 is implicated in antibody responses and SLE. The study underscores the indispensable role of TRPV2 in immune regulation and potential therapeutic interventions.

Shedding of infected enterocytes into the gut lumen is a hallmark of the adult mucosal antimicrobial response. In contrast, enterocyte shedding is rare in the neonatal intestine. Instead, we observe internalization and degradation of infected enterocytes by neighboring epithelial cells.

Monocytes restrict Yersinia infection within intestinal pyogranulomas. Here, we report that monocyte-intrinsic TNF signaling drives the production of IL-1 that signals non-hematopoietic cells to control intestinal Yersinia infection within pyogranulomas.

Proliferation of infected T cells drives HIV-1 persistence. At the single-cell level, Kufera et al. demonstrate that, independent of host immune pressure, infected CD4⁺ T cells carrying an intact HIV-1 provirus have reduced proliferative responses.

TCR signaling (signal 1) induces STAT3 phosphorylation through Lck/Fyn and, synergistically with cytokine signal (signal 3), induces optimal STAT3 phosphorylation to drive T_H17 cell differentiation. Selective inhibition of TCR stimulation–induced STAT3 phosphorylation significantly inhibits T_H17 differentiation and ameliorates T_H17 cell–related autoimmune diseases.

The study introduces a new immunotherapy for treating melanoma and other cancers by developing a PROTAC that degrades NR4A1, an intracellular nuclear factor that plays a crucial role in immune suppression.

Through integrative analyses of mouse models and clinical data, Qin et al. find that certain ALK-rearranged LUAD hold the potential toward squamous transition. Such phenotypic transition associates with TKI resistance and relies on the JAK-STAT signaling.

Microglia are thought to drive neuroinflammation in age-related macular degeneration (AMD). Here, Yu et al. identified a protective microglia population that mitigates degeneration via atrophic debris elimination in disease models. This population is present and highly conserved in human AMD.