concanavalin-a has been researched along with Genetic-Diseases--Inborn* in 1 studies
1 other study(ies) available for concanavalin-a and Genetic-Diseases--Inborn
| Article | Year |
|---|---|
CD36 deficiency attenuates immune-mediated hepatitis in mice by modulating the proapoptotic effects of CXC chemokine ligand 10.
The scavenger receptor CD36 recognizes a diverse set of ligands and has been implicated in a wide variety of normal and pathological processes, including lipid metabolism, angiogenesis, atherosclerosis, and phagocytosis. In particular, recent findings have demonstrated its crucial functions in sterile inflammation and tumor metastasis. However, the role of CD36 in immune-mediated hepatitis remains unclear. Concanavalin A (ConA)-induced liver injury is a well-established experimental T cell-mediated hepatitis. To understand the role of CD36 in hepatitis, we tested the susceptibility of CD36-deficient (CD36. Our findings suggest that CD36 plays an important proinflammatory role in ConA-induced liver injury by promoting hepatic inflammation and mediating the proapoptotic effect of chemokine CXCL10, and therefore, may be a potential therapeutic target for immune-mediated hepatitis. (Hepatology 2018;67:1943-1955). Topics: Animals; Apoptosis; Blood Platelet Disorders; CD36 Antigens; Chemical and Drug Induced Liver Injury; Chemokine CXCL10; Concanavalin A; Cytokines; Disease Models, Animal; Flow Cytometry; Genetic Diseases, Inborn; Genistein; Hepatitis; Hepatocytes; Liver; Mice; Mice, Inbred C57BL; Signal Transduction | 2018 |