Furthermore, histological
analysis indicated that IL-33 treatment exacerbated
mononuclear and polymorphonuclear cell infiltration into the joint
and synovial hyperplasia, along with significant cartilage and bone
erosion [32]. On the other hand, treatment with IL-33 was not able
to influence the incidence or severity of CIA in ST2/ mice, nor the
generation of inflammatory cytokines, suggesting that IL-33 plays a
role in RA by virtue of a ST2-dependent mechanism.