Table 1.

Immune mediators and receptors expressed by enteric neurons and their observed roles in intestinal homeostasis.

Receptor	Phenotype	References
TLR2	TLR2 −/− have reduced GDNF levels causing abnormal ENS architecture, neuronal subtype specification, delayed transit time, and abnormal mucosal secretion	[44]
TLR4	TLR4 −/− mice have prolonged intestinal motility, decreased nNOS neurons	[35]
TLR9	Promotes macrophage chemoattraction and secretion of proinflammatory cytokines.	[45]
MyD88	ENS-specific deletion of MyD88 causes prolonged intestinal motility and decreased nNOS neurons	[35]
TGR5	TGR5 −/− mice have slower colonic transit	[111]
IL-4Rα	Signaling activated by IL-4, IL-13, potentially involved in infection mediated hypermotility	[41,112,113]
TNF SRF	TNFα signaling promotes neuronal production of neuropeptide Y and influences intestinal inflammation and motility	[114]
TGFβR	TGFβ signaling induces neurite outgrowth in cultured neurons	[115]
Mediator
IL-6	Inhibits Rorγ Treg induction in a microbiota dependent manner in adults	[48]
IL-18	Induces goblet cells to produce antimicrobial peptides in adults	[49]
CSF-1	Facilitates crosstalk between ENS and macrophages, increases with age	[54]