Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the virus that causes coronavirus disease-2019 (COVID-19). The virus was first identified in December 2019, spread worldwide, and caused many deaths. The World Health Organization (WHO) declared a global public health crisis on 30 January 2020 and a pandemic on 11 March 2020. SARS-CoV-2 is a single-stranded RNA virus belonging to the genus Coronavirus and the family Coronaviridae. SARS-CoV-2 has four structural proteins, Envelope (E), Membrane (M) and Nucleocapsid (N) and Spike (S) proteins. The S protein consists of S1 and S2 subunits. The receptor-binding domain (RBD) of the virus is located in the S1 subunit and binds the virus to the surface receptor angiotensin convertase-2 (ACE2) of the host cell. This study aimed to better understand the production of proinflammatory cytokines in macrophages after in vitro interaction with the RBD of SARS-CoV-2. Gene expression of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and interleukin-1 Beta (IL-1β) in RBD stimulated mouse macrophage cell line RAW 264.7 was detected with quantitative Reverse Transcription Polymerase Chain Reaction (RT-qPCR). In addition, the concentration of secreted TNF-α, IL-6 and IL-1β was quantified with sandwich enzyme-linked immunosorbent assay (ELISA). The study indicated that mouse macrophages produce TNF-α upon exposure to SARS-CoV-2 RBD after 6 and 24 hours of cell stimulation, but neither IL-6 nor IL-1β were increased after stimulation. The future goals of the study are to understand how the immune system responds to the SARS-CoV-2 infection, and how this can help in treating COVID-19.