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. 2020 Jul 15;19(8):553–571. doi: 10.1038/s41573-020-0071-y

Table 3.

Cell lineage-specific A20 alterations in mouse models that phenocopy human inflammatory and immune diseases

Mutant type Lineage/model Phenotype Refs
A20–/– Global knockout mouse Spontaneous systemic inflammation, severe cachexia and premature lethality; survival prolonged with Ripk1D138N/D138N or Ripk3–/– mice, but not with Mlkl–/– 156,218,219
A20−/− Murine embryonic fibroblasts Sensitized to RIPK1-dependent apoptosis and necroptosis 38
A20EKO Keratinocyte-specific knockout mouse Systemic inflammation and exacerbated disease in models of psoriasis and atopic dermatitis 220
A20LysM-Cre Myeloid-specific knockout mouse Spontaneous inflammatory joint arthritis; rescued by Ripk1D138N/D138N mutation, Ripk3–/– or Mlkl–/– 80,208
A20IEC/myel-DKO IEC and myeloid-specific double-knockout mouse Intestinal pathology through synergistic IEC and myeloid mechanisms to promote ileitis and severe colitis 81
A20mZnF7/mZnF7 Global C764A;C767A ZnF7 knock-in mouse Spontaneous inflammatory arthritis with activated RIPK1 80
A20ΔIEC IEC-specific knockout mouse Hypersensitive to TNF-induced systemic inflammation; partially blocked by inhibition of RIPK1 (Ripk1D138N/D138N) 221
A20IEC-transgenic mice IEC-specific overexpression Hypersensitive to TNF-induced intestinal damage in RIPK1-dependent manner 79

IEC, intestinal epithelial cell; MLKL, mixed-lineage kinase domain-like pseudokinase; RIPK1, receptor-interacting serine/threonine-protein kinase 1; TNF, tumour necrosis factor; ZnF7, zinc finger 7.