Figure 5.

LILRB4 plays a role in transplant tolerance and maternal–fetal tolerance. In transplantation tolerance induction, upregulation of LILRB4 expression on APCs using vitamin D3, IL-10 and IFN-α or the use of recombinant LILRB4 protein induces a decrease in co-stimulatory molecules such as CD80/CD86 on APCs. It also induces Th and CTL cell dysfunction and causes expansion of Ts and Treg cells, which could be effective in inducing transplantation tolerance. This can effectively induce the generation of graft tolerance. During maternal–fetal tolerance, HLA-G is highly expressed in extrachorionic trophoblast cells, which induces upregulation of LILRB4 on uterine dendritic cells and metaplastic macrophages and induces the generation of tolerant DCs by altering the expression of cell membrane molecules such as CD80, CD86, etc. At the same time, it enhances M2-type macrophage differentiation and attenuates M1-type macrophage proliferation, through which the creation of tolerant environments could potentially lead to a pathway for congenital Toxoplasma gondii treatment and prophylaxis (illustrated using www.figdraw.com, accessed on 25 January 2024).