CCR6+ ILC3s from mice with arthritis expressed significantly higher levels of IL-17A and IL-22 mRNA than did comparable cells from control mice (p < 0.0001 and p = 0.015).
Mucosal T cell production of IL-17, interferon-γ, tumor necrosis factor α (TNFα), IL-22, and granulocyte-macrophage colony-stimulating factor (GM-CSF) was analyzed by flow cytometry and Luminex assay before arthritis onset in mice immunized to develop collagen-induced arthritis (CIA).
IL‑22 expression exhibited an increasing trend in the initial phase and the onset phase of arthritis and increased significantly with progression to chronic arthritis in the PIA rat model.
Recent findings suggest that not only the expression of IL-22 is abnormal both in RA patients and in arthritis mice but also the aberrant IL-22 performs significantly in disease onset of RA.
Relationship of CD146 expression to secretion of interleukin (IL)-17, IL-22 and interferon-γ by CD4(+) T cells in patients with inflammatory arthritis.
Remarkably, the less severe form of arthritis in IL-22(-/-) mice was associated with increased production of CII-specific and total IgG antibodies, whereas cellular CII responses were unchanged.