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Immunity to gastrointestinal nematodes in ruminants: effector cell mechanisms and cytokines
- Hendawy, Seham H. M.
- Journal of parasitic diseases 2018 v.42 no.4 pp. 471-482
- B-lymphocytes, defense mechanisms, economic impact, eosinophils, fecundity, females, gastrointestinal nematodes, host-parasite relationships, immune evasion, immune response, immunoglobulin A, immunoglobulin E, immunoglobulin G, interleukin-10, interleukin-13, interleukin-4, interleukin-5, interleukin-9, larvae, mast cells, nutrition, parasitism, parasitoses, physiological state, ruminants
- Gastrointestinal nematodes (GINs) of ruminants are prevalent and have major economic impacts worldwide. The insight studies of immune responses triggered against GINs are of great concern to understand interaction between host’s immune system and parasite. T-helper 2 cytokines drive the effector cell mechanisms which include eosinophils and mast cells. The immune responses are controlled by Th2 secreted interleukins (IL); IL3, IL-4, IL-5, IL-9, IL-10 and IL-13. B-Cell immune response is incorporated in defense mechanisms developed against GINs specially immunoglobulins (Ig); IgA, IgE and IgG. The immune resistance of the infected host is presented by failure of larval establishment or hypobiosis, low worm burden and decreased female fecundity. The host–parasite interaction is a complex series that affected by host’s genetic constitution, nutrition, age and physiological status. The GINs have different immune evasion mechanisms to improve their survival within the host. Also, management of the host influences GINs parasitism. Thus, the aim of this review is to highlight the hallmarks of immune responses that endorse GINs parasitism. The insights studies of the triggered immune responses developed against GINs will improve the appropriate protective immune strategy.