Table 1.

Selected murine enthesitis models

Reference	Species	Strain	Intervention	Characteristics
Reihardt et al. [16]	Mice	Tcrd-H2BeGFP mice crossed with mice of the susceptible B10.RIII background	Hydrodynamic injection of IL-23 minicircle DNA	Activated Vγ6+CD27− γ/δ T cells were found in uninflamed entheseal tissue and constituted the largest resident T cell subset.
Armaka et al. [59•]	Mice	TNF-overexpressing mouse model (TNFΔARE/+)		Spondyloarthritis with a CD-like pathology localized primarily in the small intestine. Additionally, the development of arthritis was dependent on TNF receptor I (TNFRI) expression with mesenchymal cells being primary responders.
De wilde et al. [24]	Mice	A20myelKO mice	A20 knockout	Enthesitis was found to be an early inflammatory lesion in A20myelKO mice. A20 negatively modulated STAT1-dependent gene transcription in myeloid cells which was JAK/STAT dependent.
Benham et al. [15]	Mice	BALB/c ZAP-70(W163C)-mutant (SKG) mice	β-1,3-Glucan injected intraperitoneally	In curdlan-treated SKG mice, arthritis, enthesitis, and ileitis were IL-23 dependent. Enthesitis was specifically dependent on IL-17A and IL-22. IL-17A was pathogenic, while IL-22 was protective against ileitis.
Sherlock et al. [8]	Mice	B10.RIII mice	Immunization with type II collagen	IL-23 is essential in enthesitis and acts on previously unidentified IL-23 receptor (IL-23R)+, RAR-related orphan receptor gt (ROR-gt)+CD3+CD4–CD8–, stem cell antigen 1 (Sca1)+ entheseal resident T cells which led to the induction of IL-6, IL-17, and IL-22 as well as of CXCL1 secretion leading to osteoblast remodeling which is characteristic of enthesitis.