Table 2.
Mouse models in the research of GCA pathogenesis.
Animal Model | Mechanism of Action | Limitations | Ref, Year |
---|---|---|---|
Human artery engraft | in NOD-SCID mice | leakage, spontaneous thymomas, very short lifespans | [212], 1997 [185], 2017 |
Induction of arteritis through administration of TLRs and activation of adventitial DCs | at the vasa vasorum | technically challenging for rodents | [214], 2022 [215], 2003 |
at perivascular adipose tissue (PVAT) | involvement in atherosclerosis, speculation for GCA pathogenesis | [219], 2022 [220], 2000 [221], 2005 |
|
Induction of arterial injury through arterial cuffing | in genetically modified atherosclerosis-prone mice | speculation for GCA pathogenesis | [216], 2002 |
in IBP-deficient or IL-1Ra deficient mice | not sufficient to initiate pan-arteritis | [217], 2003 [218], 2014 |
|
Induction of arterial injury through intraluminal balloon | in atherosclerotic mice | tested in mouse and rat models of atherosclerosis, speculation for GCA pathogenesis | [222], 2007 |
Modified arteritis-prone models | IL1-A deficiency mice upon artery injury | arteritis development is dependent on the genetic background | [223], 2005 |
or IL25 administration | speculation for GCA pathogenesis | [224], 2019 | |
IBP-deficient mice with TCR specific to OVA peptides | speculation for GCA pathogenesis | [225], 2008 | |
Infection-related chronic vasculitis | IFNg-receptor-deficient mice infected with γ-herpes virus 68 | IFNg signaling deficiency not investigated in LVV patients | [226], 2001 [227], 1998 |