CD137 receptor, belonging to Tumor necrosis factor receptor superfamily 9, classifies as a CD marker resting on the surface of the cell. Its function involves both nonimmune and immune cells, such as cellular apoptosis, survival, differentiation, proliferation, and also activation. We postulated that the interaction between the CD137 receptor and CD137 ligand leads to cellular apoptosis in particular cells. Most of the severe patients with Dengue virus infection demonstrated the apoptotic body containing hepatocytes. In our earlier reports, we revealed that infection of Dengue virus in hepatocyte cell line stimulated the expression of CD137 receptor in both mRNA and surface protein expression levels, which related to enhanced apoptosis in Dengue-infected hepatocytes. This mechanism might be the pathogenesis of apoptosis in the hepatocytes of the patient with severe Dengue infection and still has not been elucidated. Nevertheless, we noticed the pivotal role of the mechanisms of the CD137 receptor that leads to apoptosis in Dengue-infected hepatocytes. The purpose of this research is to produce the expression recombinant plasmid containing CD137 receptor gene by using Recombinant DNA technology to test its function upon Dengue-infected hepatocytes later. Recombinant DNA technology is usually employed with the advantage of easy handling and low cost. Amplification of insert CD137 receptor gene was done by using Nested PCR. Plasmid and insert DNA were double-digested with restriction endonuclease enzymes and subjected to ligate. Then, transformation into competent bacteria was performed and selected the white colonies on Ampicillin-containing media. Screening methods and direct sequencing were utilized to verify the correct base pairing sequence. Our result demonstrated the accomplishment in the construction of recombinant plasmid comprising CD137 receptor with completely matched to its template in GenBank and it will be employed in further study in surface CD137 receptor expression in protein level and functional level during DENV-infected hepatocytic cell line.