Table 1 IL-22 dysregulated in CTDs and possible underlying mechanisms
From: Interleukin-22 and connective tissue diseases: emerging role in pathogenesis and therapy
CTDs | Samples examined | Changes of IL-22 level | Research model | Mechanism | Refs. |
|---|---|---|---|---|---|
SLE | PBMCs | ↑ | Human (LS) | Up-regulate the expression of IL-22R1 on the keratinocytes | [28] |
Activate ICAM-1 by TNF-α | [29] | ||||
↓ | Human (LN) | Decrease TNF-α level | [30] | ||
ND | Human | CNV of IL-22 gene | [34] | ||
Serum/kidney | ↑ | Human (LN), MRL/lpr mice | ND | [31] | |
T cells | ↑ | Human | Destroy PD-1 pathway by TGF-β1 | [32] | |
RA | Synovial tissues | ↑ | Human, C57BL/6 mice | Enhance the production of MMP1 and S100A8/A9 | [42] |
Stimulate production of MCP-1 | [48] | ||||
Increase pro-inflammatory mediators | [49] | ||||
Suppress anti-inflammatory IFN-É£ responses | [50] | ||||
Heighten IL-22 effects by TNF-É‘, exogenous and endogenous ligands of TLR3 and TLR4 | [42] | ||||
SS | Salivary glands | ↑ | Human | Product several cytokines and chemokines (i.e. CXCL13 and CXCL12) | [65] |
Aberrant expression of IL-22R1 on haematopoietic cells | [66] | ||||
SSc | Skin | ↑ | Human | The TNF/IL-22 axis and their receptors, together with TGF-β, in part, constituted the existing inflammatory component of SSc | [72] |
Downregulate let-7a | [77] | ||||
DM | Muscle biopsies | ↑ | Human | IL-22/IL-22R/STAT3 pathway | [88] |