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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-ɣ responses [50]
Heighten IL-22 effects by TNF-ɑ, 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]
  1. ↑: upregulation; ↓: downregulation; ND not determined