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Table 1 Potential effects of absent in melanoma 2 (AIM2) inhibition on RA

From: Absent in melanoma 2 (AIM2) in rheumatoid arthritis: novel molecular insights and implications

Cell populations

The potential effects of inhibition of AIM2

References

T-cell subsets

AIM2 inhibition may alleviate rheumatoid arthritis (RA) by suppressing excessive apoptosis of T cells

[31, 32]

AIM2 inhibition may inhibit autoimmune T-cell development and function, suppressing excessive inflammatory responses

[33, 34]

AIM2 inhibition in Treg cells may lead to their functional defects. In addition, inhibition of AIM2 by some microRNA long noncoding RNA interactions may affect the balance between Treg/ T helper 17 (Th17) cells

[35, 38]

B-cell subsets

AIM2 inhibition of the cluster of differentiation(CD)27 + B cells may promote the release of the anti-inflammatory factor IL-10 and inhibit pyroptosis from suppressing inflammation

[39, 41, 42]

AIM2 inhibition may affect B-cell differentiation by regulating The B cell lymphoma 6 (BCL6)-B-lymphocyte-induced maturation protein 1 (BLIMP1) expression

[44]

Fibroblast-like synoviocytes (FLS)

AIM2 inhibition may inhibit FLS hyperproliferation and inflammatory responses. In addition, AIM2 inhibition may affect RA-associated atherosclerosis by regulating oxidized low-density lipoprotein (ox-LDL) and gasdermin D (GSDMD)-N

[53, 60]

Monocytes

AIM2 inhibition in monocytes may promote their survival and facilitate differentiation to pro-inflammatory cells, thereby exacerbating the inflammatory process

[61]

Macrophages

AIM2 inhibition in macrophages reduces the activation of pyroptosis and promotes autophagy to reduce the inflammatory response

[63, 79]