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Published on: February 10, 2015
ICOSL deficiency promotes M1 polarization to alleviate liver fibrosis in schistosomiasis mice
Lei Liu1, Peng Wang2, Shi-Qi Xie3
1Department of Parasitology, Medical College of Soochow University, 199 Renai Road, Suzhou 215123, Jiangsu, China; Department of Blood Transfusion, The First Affiliated Hospital of University of Science and Technology of China, 17 Lujiang Road, Hefei 230032, Anhui, China.
The expression of inducible co-stimulator ligand (ICOSL) on macrophage (Mφ) implies their ability to interact with inducible co-stimulator (ICOS)-expressing T cells, thereby modulating immune responses within the liver microenvironment. This study aimed to elucidate the mechanism underlying ICOS/ICOSL signaling in the regulation of Mφ polarization during Schistosomiasis-induced liver fibrosis. To investigate this, ICOSL-knock out (KO) and wildtype (WT) C57BL/6 mice were infected with Schistosoma japonicum (S. japonicum) to examine the dynamic changes in Mφ phenotype and observe the pathology alterations in the liver. There was significantly decreased expression of ICOSL both in monocytes of cirrhosis patients and the liver tissue of mice infected with S. japonicum. Furthermore, ICOSL-KO mice exhibited reduced liver granuloma formation and fibrosis during S. japonicum infection. Simultaneously, Mφ in ICOSL-KO mice polarized towards M1-type and induced apoptosis of hepatic stellate cells (HSCs). Overall, the blockade of ICOSL signaling could promote M1 polarization, induce HSCs apoptosis, and ameliorate hepatic fibrosis, suggesting that ICOSL may serve as a potential biomarker for prognosis and therapeutic target for schistosomiasis-induced hepatic fibrosis.
The expression of inducible co-stimulator ligand (ICOSL) on macrophage (Mφ) implies their ability to interact with inducible co-stimulator (ICOS)-expressing T cells, thereby modulating immune responses within the liver microenvironment. This study aimed to elucidate the mechanism underlying ICOS/ICOSL signaling in the regulation of Mφ polarization during Schistosomiasis-induced liver fibrosis. To investigate this, ICOSL-knock out (KO) and wildtype (WT) C57BL/6 mice were infected with Schistosoma japonicum (S. japonicum) to examine the dynamic changes in Mφ phenotype and observe the pathology alterations in the liver. There was significantly decreased expression of ICOSL both in monocytes of cirrhosis patients and the liver tissue of mice infected with S. japonicum. Furthermore, ICOSL-KO mice exhibited reduced liver granuloma formation and fibrosis during S. japonicum infection. Simultaneously, Mφ in ICOSL-KO mice polarized towards M1-type and induced apoptosis of hepatic stellate cells (HSCs). Overall, the blockade of ICOSL signaling could promote M1 polarization, induce HSCs apoptosis, and ameliorate hepatic fibrosis, suggesting that ICOSL may serve as a potential biomarker for prognosis and therapeutic target for schistosomiasis-induced hepatic fibrosis.
