Fasciolosis of Ruminants: immunity, immunomodulation and control strategie | La fasciolose des ruminants : immunité, immunomodulation et stratégie de prévention

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anglais. The first part of this article describes the differences in immune response against the liver fluke found in its various ruminant hosts. It shows that sensitivity to F. hepatica and F. gigantica infestation and the development of a resistance against these parasites vary widely from host to host. These host-specific responses of against the parasite, and especially the cellular response, are described. Lesions form around a necrotic area with inflammatory cells organised into a granuloma. These cells are mainly macrophages, lymphocytes and eosinophil granulocytes;the excretion-secretion products of F. hepatica or F. gigantica trigger early on a proliferative response from lymphocytes, as well as a secretion of cytokines, which vary depending on the ruminant host. The elimination of Fasciola spp. during its peritoneal or hepatic migration involves two mechanisms: destruction by macrophages activated by interferon gamma, which produces nitrogen monoxide (NO) toxic for the parasite, and antibody-dependent cellmediated cytotoxicity (ADCC). These mechanisms are dependent on either Th1 cytokines, particularly IFNγ for the induction of NO, or Th2 cytokines for ADCC. We describe how the parasites defeat these two mechanisms. This phenomenon could explain why ruminant resistance to reinfestation is only limited and why there is no premunition against flukes. Consequently, the anti-fasciolosis strategy is directed at the parasite, using agronomic measures to prevent animal infestation. Given the type of immunity animals develop against fasciolosis, the efficacy of vaccines is limited to reducing the parasite load.