| Objective To observe the way and the mechanism of T follicular helper cellpromote the formation of granulomas during Schistosoma japonicum infection.Method Liver granulomas of C57/BL6mice after Schistosoma japonicuminfection were isolated to analyze by hematoxylin-eosin staining and cell count.Tfollicular helper cell in spleenã€lymph node and liver and eosinophil in chemotaxisassays were determined by FACS respectively. Results Compared to wild typemice, after Schistosoma japonicum infection,the total number of liver granulomasfrom ICOSL-knock out mice decreased significantly and the number and ratio ofeosinophil in liver granulomas also significant decreased(P<0.05, P<0.001,P<0.05).Eosinophil express chemokine receptor CXCR4while T follicular helper cell secreteCXCL12, the ligand of CXCR4(P<0.001, P<0.001). In vitro chemotaxis assay,eosinophil migrated to the bottom well in respond to T follicular helper cell andCXCL12neutralizing antibody could effectively attenuate the chemotaxis (P<0.001).Conclusion After Schistosoma japonicum infection, liver granulomas formed inC57/BL6mice, the number of eosinophil in liver and T follicular helper cell inimmune tissues increseaed. Our results demonstrated that, by its combination withreceptors, CXCL12played a significant chemotactic role on the migration ofeosinophil. This indicates a possible role of T follicular helper cell on the migrationof eosinophil by secretion of CXCL12. |