Fasting-activated VLM-CA neurons suppress autoimmune disease!

Feeding behavior is one of the most fundamental needs for animals, and perform a huge impact on immune system. In situations of energy deficiency, the bone marrow is considered as a "safe haven" for immune cells. When the body experiences energy insufficiency, the immune cells begin to traffic back to the bone marrow, which called "homing", and turn into a relatively quiescent state.

Our latest research reveals that dietary restriction can activate catecholaminergic neurons in the ventrolateral medulla (VLM-CA) of the brainstem. By promoting T cell homing, it suppresses the activation, proliferation, and differentiation of T cells in experimental autoimmune encephalomyelitis (EAE) mice, thereby improving autoimmune diseases.

Our groundbreaking discovery demonstrates that activation of hunger-sensing VLM-CA neurons can upregulate the CXCR4/CXCL12 signaling pathway, thereby driving T cell homing to the bone marrow and inhibiting autoimmune inflammation. Targeting VLM-CA neurons, we envision the development of safe methods to specifically modulate their activity and shed a light on the treatment of autoimmune diseases and hyperinflammatory conditions.

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links:https://www.nature.com/articles/s41593-023-01543-w