A wide range of plant viruses constitute an important category of pathogens. Although most known plant viruses have a very limited host range, they lead to the symptomatic phenotypes of disease in many cases and cause enormous losses in agricultural economy by reducing crop yield and quality of important economic plant products. Despite the simple genomes of viruses, the molecular basis for viral pathogen detection and immune signaling activation in plant hosts are not well elucidated. In recent years, it was illustrated that plants have evolved complicated defense mechanisms to counteract virus attack, which can generally be classified into two strategies: protein-mediated and RNA silencing-based defenses. Protein based antiviral immunity relies on various immune receptors encoded by the host, which mainly constitute by pattern recognition receptors (PRRs) and resistance (R) proteins. Currently, no specific PRR but a few typical co-receptors such as BAK1 have been identified to fight against viral pathogens and induce a series of PTI responses, suggesting PRR triggered immunity (PTI) functions in defense against viral infection. In addition, resistance (R) protein-mediated immune response termed as effector triggered immunity (ETI) against viral pathogens is far more robust, in most cases limiting viral replication and systemic spreading. The transmembrane receptor-like kinase nuclear shuttle protein (NSP)-interacting kinase 1 (NIK1) mediates a new antiviral defense mechanism against begomovirus through suppression of translation in plants, which is completely different from BAK1-mediated PTI despite their similar structures. RNA silencing, also termed as RNA interference (RNAi), acts as the basal and adaptive defense against viral invasion, which also is the primary plant antiviral mechanism. RNAi relies on siRNAs from the processing of viral dsRNAs by ribonuclease type III Dicer-like (DCL) proteins. The siRNA is assembled into RNA-induced silencing complex (RISC) containing core component Argonaute to guide RISC to the target viral RNA which contains complementary sequence. Consequently, viral RNAs are degraded by the Argonaute of RISC. Inplants, DCL2 and DCL4 which generate 22-nt and 21-nt siRNA respectively are required for antiviral immunity. The current model states that the two DCLs act in a redundant, but hierarchical way in antiviral silencing, with DCL4 as the predominant antiviral Dicer protein. However, the functional mechanism of DCL2 in resistance to viral infection in plants is still elusive. This work investigates the antiviral mechanism of DCL2 in Arabidopsis. We proposed DCL2 functions as a co-receptor for certain R protein (RDCL2). DCL2 senses accumulation of viral RNA in the cell only when the RNA silencing by DCL4 is lost, and activates RDCL2 mediated immune responses. In this work, we showed that dcl4 was a DCL2 dosage dependent auto-immune mutant. By transgenic expression of dominant negative version of conserved R genes of NB-LRR type, two genes AT1G12290 and AT1G31540, which we called as R4 and R79 were identified as DCL2 co-receptors. In addition, another candidate RDCL2 gene AT4G12010 which we called as R78 has been screened recently and is under further verification. Moreover, we provided evidence that R4 and R79 played the role of viral resistance by cooperating with DCL2. We also managed to uncouple the dicing and sensing activities of DCL2 by G898E substitution in the PAZ domain. Finally, the physical interaction of DCL2 with R4 and R79 was examined, and our preliminary data indicated that DCL2 likely interacted with R79 but not with R4.