The spider mites Tetranychus evansi Baker & Pritchard and Tetranychus urticae Koch (Acari: Tetranychidae) are key tomato pests worldwide. Biological control of spider mites using phytoseiid predatory mites remains challenging. The glandular trichomes on the tomato leaves and stem severely hamper the movement and establishment of the predatory mites. As a result, smaller predatory mites, able to thrive under the sticky heads of the glandular trichomes, have gained much interest. As some iolinid predatory mites were reported to feed on spider mites, we investigated the potential of Pronematus ubiquitus McGregor to control both T. urticae and T. evansi on tomato plants. On whole tomato plants, P. ubiquitus was able to suppress populations of T. urticae, but not of T. evansi. Based on the marginal number of spider mites killed in laboratory trials, the observed biocontrol effect on full tomato plants might not be due to direct predation but to a plant-mediated indirect impact. The oviposition of T. urticae was found to be significantly lower on tomato leaflets pre-exposed to P. ubiquitus as compared to non-exposed leaflets. The oviposition rate of T. evansi was not affected by previous exposure of the tomato host plant to P. ubiquitus. We demonstrated that P. ubiquitus reduces the population growth of T. urticae on tomato plants. Further large-scale field trials need to confirm the findings of the present study.

By mirroring their function as tissue repair organizers in normal tissues, immune cells regulate tumor growth. To understand the different facets of immune-tumor collaboration through genetics, spatial transcriptomics, and immunological manipulation with non-invasive, longitudinal imaging, we generated a penetrant double oncogene-driven autochthonous model of neuroblastoma. Using spatial transcriptomic analysis, we co-localized CD4+ and myeloid populations within the tumor parenchyma, while CD8+ T cells and B cells were peripherally dispersed. Depletion of CD4+ T cells or CCR2+ macrophages, but not B cells, CD8+, or NK cells, prevented tumor formation. Tumor CD4+ T cells displayed unconventional phenotypes, were clonotypically diverse, and antigen-independent. Within the myeloid fraction, tumor growth required myeloid cells expressing Arginase-1. Overall, our results suggest that arginine-metabolizing myeloid cells conspire with pathogenic CD4+ T cells to create permissive conditions for tumor formation, and therefore suggest that these pro-tumorigenic pathways can be disabled by targeting myeloid amino acid metabolism.