Figure 3.
BMAL1-dependent tumor programs in myeloid cells. Loss of BMAL1 disrupts key functional programs in neutrophils and macrophages, as well as within the TME, underscoring the critical role of CRs in regulating both pro- and anti-tumoral myeloid responses. Neus, neutrophils. The process is depicted within a circular tissue field, showing that B M A L 1 regulates key functional programs in macrophages and neutrophils. On the macrophage side, the diagram highlights the impact on P D-L 1 levels, M H C-2 expression, and C D 8 plus T cell priming, as well as impaired mitochondrial function and reduced phagocytosis. On the neutrophil side, it showcases N E T formation, E C M production, and metabolic reprogramming contributing to a pre-metastatic niche. Central to the diagram are the roles of lipid availability and the H I F-1 alpha program in shaping the LLM phenotype (T R E M 2 plus C D 36 plus G P M N B plus). Finally, the bottom of the graphic shows how these processes are tied to time, illustrating the rhythmic production of cytokines like I L-1 beta and I L-6, thereby underscoring the role of circadian rhythms in modulating pro- and anti-tumoral myeloid responses.

BMAL1-dependent tumor programs in myeloid cells. Loss of BMAL1 disrupts key functional programs in neutrophils and macrophages, as well as within the TME, underscoring the critical role of CRs in regulating both pro- and anti-tumoral myeloid responses. Neus, neutrophils.

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