Fig. 1

Functional diagram of the model representing the within-host immune response to PRRSv infection. Functional diagram of the model representing the within-host immune response to PRRSv infection. Binding of PRRS viral particles (V) and naive target cells (T_n) either result in mature and non-infected cells (T_m) that phagocytes viral particles, or in mature and infected cells (T_i) that allows viral replication and excretion of new viral particles. Phagocytosis is amplified by antiviral cytokines (TNFα, IFNα, IFNγ) and inhibited by immuno-modulatory (IL10, TGFβ) cytokines; on the contrary, infection and viral replication are inhibited by antiviral cytokines and amplified by immuno-modulatory cytokines. TNFα induces the apoptosis of T_n, T_m and T_i. Viral particles are neutralised by antibodies (nAb); infected cells are cytolysed by natural killers (NK) and Cytotoxic T Lymphocytes (CTL). Mature target cells (T_m and T_i) synthesise cytokines and present the viral antigen to naive adaptive effectors (En, not explicitly represented in the model). Once activated, they differentiate into cellular (E_c), humoral (E_h) or regulatory (E_r) effectors, depending on the cytokinic environment. Pro-cellular regulatory cytokines (IFNγ, IL12) favour E_c, whereas pro-humoral regulatory cytokines (IL4, IL6) E_h and pro-regulatory regulatory cytokines (TGFβ) E_r. These effectors synthesise cytokines and induce the activation of plasma cells (B), which synthesise nAb. Moreover, E_c induce the activation of CTL. Finally, the recruitment of T_n and NK is amplified by pro-inflammatory cytokines (Pi, which groups IL1β, IL6, IL8 and CCL2). Colours – green: PRRSv particles; red: innate response; blue: adaptive response; purple: both innate and adaptive responses. Lines – plain with arrow: state changes; dashed (dotted) with arrow: (cytokine) syntheses; plain dark grey with ⊕: up-regulations by cytokines; plain light grey with ⊖: down-regulations by cytokines