Bruce Levine, Barbara and Edward Netter Professor in Cancer Gene Therapy at the University of Pennsylvania, shared a post on X:
“A tumor-brain interface?
Tumor-brain crosstalk restrains cancer immunity via a sensory-sympathetic axis – lung tumors in mice can co-opt the nervous system to weaken local immunity Tumor → nerve → brain: Lung tumors recruit a specific vagal sensory subtype that carries signals to the brainstem.
Brain → nerve → tumor: Brainstem circuits increase sympathetic outflow back to the tumor. Immune consequence: Sympathetic neurotransmission (noradrenaline) engages β2-adrenergic signaling in alveolar macrophages, shifting them toward an immune-suppressive state and reducing effective anti-tumor T cell activity.
Causality: Disrupting sensory input, brainstem relay nodes, or downstream sympathetic/β2 signaling reduces tumor growth in mouse models, β2 agonism can restore tumor-promoting effects.
Why it matters: It expands “microenvironment” to include neural circuits and suggests that carefully targeted adrenergic modulation might complement immunotherapy in solid tumors.”
Title: Tumor–brain crosstalk restrains cancer immunity via a sensory–sympathetic axis
Authors: Haohan K. Wei, Chuyue D. Yu, Bo Hu, Xing Zeng, Hiroshi Ichise, Liang Li, Yu Wang, Ruiqi L. Wang, Ronald N. Germain, Rui B. Chang, Chengcheng Jin
Read The Full Article
More posts featuring Bruce Levine on OncoDaily.
