Table 3.

Strategies for the treatment of OA pain targeting neuroimmunity.

Targets		Promising Therapeutic Measures
Immune Cells	Macrophages	Inhibition of M1 polarization and induction of M2 polarization within the joint and DRG [35,27].
	Neutrophils	Neutralizing NE in the joint [81].
	T cells	Inhibition of Th17 cell differentiation [82]. Induction of Treg cell differentiation [83].
Neuronal Surface Receptors	TrkA	Blocking the binding of NGF to TrkA [84].
	TLRs	Inhibition of TLRs activation [71].
	TRPV1	Injection of high-purity synthetic trans-capsaicin into the joint [85].

OA, osteoarthritis; TrkA, tropomyosin receptor kinase A; TLRs, toll-like receptors; TRPV1, transient receptor potential vanilloid 1; DRG, dorsal root ganglion; NE, neutrophil elastase; Th17, T-helper 17; Treg cell, regulatory T cell; NGF, nerve growth factor.