Interleukin-13 in the skin and interferon-gamma in the liver are key players in immune protection in human schistosomiasis.
Dessein A,
Kouriba B,
Eboumbou C,
Dessein H,
Argiro L,
Marquet S,
Elwali NE,
Rodrigues V,
Li Y,
Doumbo O,
Chevillard C.
Immunology and Genetics of Parasitic Diseases, INSERM, Faculté de Médecine, Marseille, France. alain.dessein@medecine.univ-rs.fr
Immunity against schistosomes includes anti-infection immunity, which is mainly active against invading larvae in the skin, and anti-disease immunity, which controls abnormal fibrosis in tissues invaded by schistosome eggs. Anti-infection immunity is T-helper 2 (Th2) cell-dependent and is controlled by a major genetic locus that is located near the Th2 cytokine locus on chromosome 5q31-q33. Mutations in the gene encoding interleukin (IL)-13 that decrease or increase IL-13 production account, at least in part, for that genetic control. In contrast, protection against hepatic fibrosis is dependent on interferon (IFN)-gamma and is controlled by a major genetic locus that is located on 6q23, near the gene encoding the IFN-gamma receptor beta chain. Mutations that modulate IFN-gamma gene transcription are associated with different susceptibility to disease. These data indicate that IL-13 in the skin and IFN-gamma in the liver are key players in protective immunity against schistosomes. These roles relate to the high anti-fibrogenic activities of IFN-gamma and to the unique ability of IL-13 in Th2 priming in the skin and in the mobilization of eosinophils in tissues. The coexistence of strong IFN-gamma and IL-13-mediated immune responses in the same subject may involve the compartmentalization of the anti-schistosome immune response between the skin and the liver.
PMID: 15361241 [PubMed - indexed for MEDLINE]