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Monocytes and macrophages are privileged targets of T-2, enough to control the principal mediators of inflammation ( A pre-exposure to nanomolar T-2 concentrations reduces nitric oxide (NO) production and cell viability in the porcine alveolar macrophages activated by TLR-4 and TLR-2/6 agonists (Table 2) ( Deoxynivalenol (DON) DON or vomitoxin disturbs oxidative status in rainbow trout at concentrations below the limit fixed by the European Commission (113)

271,272 These pathways can be manipulated using agonists/antagonists, as well as molecular adaptors such as miRNAs to alleviate inflammatory reactions