Immune signaling

Immune signaling is the exchange of chemical messages, mainly cytokines and chemokines, by which immune cells coordinate the detection of threats and the mounting and resolution of inflammation.

When tissue is injured or infected, resident cells such as macrophages and mast cells release messengers including interleukin-1, interleukin-6 and tumor necrosis factor alpha. These act on nearby blood vessels and recruit further immune cells, producing the redness, warmth, swelling and pain of inflammation. Inside cells, pathways such as NF-kB and the NLRP3 inflammasome switch these messengers on, while anti-inflammatory signals such as interleukin-10 and specialized resolving lipids switch them off once the threat is contained.

Signaling that fails to resolve underlies chronic inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease and some skin disorders, and many modern medicines work by blocking specific messengers. In research, immune signaling is measured by the concentration of cytokines in blood or tissue and by markers of pathway activity. Immune cells carry CB2 receptors and other cannabinoid targets, and cannabinoids have been studied for effects on cytokine release in cell and animal work; human evidence is preclinical and early.