Expression of fibrinogen-like protein 2 (Fgl2) on Toll-like receptor 9 (TLR9) expression in autoimmune myelitis

Toll-like receptor 9 (TLR9) can participate in the signal transduction of activated immune cells and induce myelitis and other autoimmune diseases. The effector molecule fibrin-like protein 2 (Fgl2) plays a role in regulating the body's autoimmune signaling pathway. They both have the conditions for the treatment of this disease target. The objective of this work was to investigate the effect of Fgl2 on the expression of DNA receptor TLR9 in autoimmune myelitis. 140 rats were randomly divided into a normal control group, an autoimmune myelitis group, a low-dose Fgl2 group, a middle-dose Fgl2 group, a higher-dose Fgl2 group, a high-dose Fgl2 group, and a methylprednisolone group. Different injection methods were used in each group. The changes of rat behavior and disease were recorded, and brain and spinal cord tissue slices were made for observation. The results showed that in the high dose Fgl2 group, the incidence of disease was 15 %, the nerve injury score was 1.0 +/- 0.15, the body weight change was-5.8 +/- 1.24 g, the number of spinal cord tissue injury was 1.82 +/- 0.44, the number of TLR9 positive cells in the brain tissue was 7.53 +/- 1.84, and the number of TLR9 positive cells in spinal cord tissue was 5.02 +/- 1.81. These indexes were lower than those in other Fgl2 groups and significantly lower than those in autoimmune myelitis group (P < 0.05). The average incubation period of the disease was 13.66 +/- 0.41 days, which was significantly higher than that of the autoimmune myelitis group (P < 0.05). It can be observed that TLR9 signaling pathway played an important role in the occurrence and development of autoimmune myelitis. With the increase of Fgl2 dose, the number of TLR9 positive cells decreased gradually. Fgl2 treatment can reduce the expression of inflammatory factors and the severity of dysfunction in autoimmune myelitis, inhibit the expression of TLR9, and improve the condition of autoimmune myelitis.