Figure 4.

Diverse uses of LILRB4 in autoimmune diseases. In systemic lupus erythematosus (SLE), the plasma cells of SLE patients express high levels of LILRB4. Fibronectin (FN) has the property pathogenicity when it binds to LILRB4, present at high levels, in plasma cells. When FN binding to LILRB4 is blocked by a monoclonal antibody against LILRB4 or the recombinant protein of LILRB4, the increase in the levels of pathogenic autoantibody IgG is significantly inhibited, and the amount of protective antibody IgM is increased, thereby alleviating the disease. In both multiple sclerosis and inflammatory bowel disease (IBD), LILRB4 exhibits roles that are distinct from those in SLE. In MS, increased levels of LILRB4 on APCs can be induced by the use of IFN-β and vitamin D, which can reduce the production of proinflammatory cytokines and effectively suppress disease progression. In IBD, LILRB4, which is expressed on macrophages, can reduce the activation of proinflammatory cytokines by negatively regulating the activation of ERK and NF-κB signaling pathways, and it may also alleviate disease (illustrated using www.figdraw.com, accessed on 25 January 2024).